The Connection Between Parkinson’s and Lewy Body Dementia
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Dementia is not technically a diagnosis in conventional medicine. Rather, it’s a term that’s used to describe a set of symptoms that involve the following:
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Memory decline
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Reasoning decline
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Difficulty thinking
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Difficulty performing other cognitive functions
In order to diagnose a patient with a type of dementia, there must be memory problems and at least one other issue affecting the patient’s cognition such as language disturbances, movement issues, failure to recognize familiar objects, and disturbances in planning, organizing, sequencing, or abstracting information. These deficits in memory and cognition must interfere with the patient’s occupational and social function. There must also be some kind of evidence of systemic health problems or a brain disorder as the primary underlying cause of the cognitive deficits using through diagnostic neuroimaging tests.
Neuroimaging is a standard part of the protocol for doctors in developed nations of the world to detect conditions like subdural hematomas, cerebral infarcts or tumors, and normal pressure hydrocephalus that can produce symptoms similar to dementia. Lab work should also be done to determine if the patient has depression, vitamin B12 deficiency, or hypothyroidism because these issues also look and seem like dementia in terms of signs and symptoms.
In fact, studies have reported that the frequency of reversible dementias among patients who are diagnosed with an irreversible type of dementia is between 0 to 23%. So below, we’ll talk about dementia in conventional medicine and reasons why you should question a diagnosis of dementia and seek out alternative treatments that may be more effective than what the doctor is prescribing.
In a previous article about disease family trees, we talked about how it could be difficult to find information about Lewy body dementia research cure options, but how you could look instead for research talking about a Parkinson's disease cure instead because these two types of dementia share many things in common. But Parkinson’s and Lewy body dementia are not the only types of dementia that can be hard to differentiate using only symptom comparison without high-tech equipment.
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Alzheimer’s disease tends to begin with memory issues while Lewy body dementia starts with hallucinations. Parkinson’s may begin with movement related symptoms first which makes it stand out a bit from Lewy body dementia and Alzheimer’s, though in practice, it might not be easy to determine which is which.
Parkinson’s disease is caused by the loss of dopamine-producing neurons in the substantia nigra. The substantia nigra is a part of the brain that plays a critical role in reward and movement. Lewy body dementia shares a number of clinical, neuropsychological, and pathological features with Parkinson’s disease, but it involves more than one part of the brain and more than one type of cell (dopaminergic and cholinergic cells). The differences between Parkinson’s disease and Lewy body dementia (and between Lewy body dementia or Parkinson’s and Alzheimer’s) is important if you are seeking stem cell treatment, for example. Stem cells work best when the treatment is very targeted within a discreet area on just one type of cell. But other types of treatments for dementia have a more holistic effect on nervous system healing. For this reason, it isn’t always essential to have access to high-tech diagnostic equipment or to receive a very definitive diagnosis in order to get started treating neurodegenerative disease symptoms.
Scientists who study neurodegenerative disorders have noted that correctly diagnosing “dementia with Lewy bodies / DLB” is challenging and many patients who show symptoms of this disease are misdiagnosed as having Parkinson’s. What’s the point of differentiating between two diseases that are so similar? If doctors can’t tell the difference between PD and LBD, why are they regarded as different diseases?
One-Pill-for-One-Disease
The answer to that question has to do, in part, with the One-Pill-for-One-Disease paradigm that Big Pharma developed many years ago as a way to market conventional medicine. As a result of the marketing that’s been done over the years, there is a quiet, unspoken belief that, when you go to the doctor, he or she will be able to prescribe a pill, just one pill, that you will take to overcome your diseased state. Indeed, this idea of One-Pill-for-One-Disease, has been propagated in part by combining drugs into one pill when two or more drugs are normally prescribed together by doctors. Of course, simplicity can be beneficial. Patients don’t always follow their doctor’s orders even when there is only one pill involved in their treatment. But the idea here is that, if there is only One-Pill-for-One-Disease, you have to have a lot of different diseases – or rather, a lot of different diagnostic labels in order to ensure that patients receive a drug that targets the specific presentation of disease that’s manifesting in their body.
Unfortunately though, this One-Pill-for-One-Disease paradigm is often more about making profit than about finding the perfect drug to fit a particular disease. The One-Pill-for-One-Disease idea was meant to simplify medicine, but often, it creates a muddled mess. For example, is Lewy body dementia actually different from Parkinson’s disease or are these two diseases actually made up of the same underlying physical issues? The One-Pill-for-One-Disease also really hijacks the reality that sick people often need lifestyle and diet changes that involve something much more involved than just taking one pill.
Different Types of Dementia
The gold standard for diagnosing dementia with Lewy bodies is a PET scan and single-photo emission computed tomography (SPECT) tracers. Dopamine transporter loss in the brain is the signature feature of LBD in conventional medicine. As LBD progresses, it impacts a bigger area of the brain than PD, though in Alzheimer’s, brain damage can impact a larger area similar to what’s observed in LBD. The loss of dopamine transporters in LBD helps to differentiate this disease from other types of dementia such as Alzheimer’s, but Alzheimer's is a neurodegenerative brain disorder that mostly impacts memory and language. In contrast, PD tends to impact movement and coordination while LBD involves hallucinations and REM sleep disorder. Alzheimer’s begins with memory loss, but Parkinson’s patients typically complain about physical stiffness and tremors as their first set of symptoms. LBD patients begin with symptoms that resemble Alzheimer’s, but the disease progresses more in the direction of eventual Parkinson’s symptoms. Alzheimer’s patients, in contrast, are unlikely to eventually develop movement-related issues.
Frontotemporal dementia and Alzheimer’s disease are similar, but they affect different regions of the brain. Frontotemporal dementia, as the name suggests, impacts the front of the brain including the frontal and the temporal lobes. These areas of the brain are associated with personality, behavior, and language, as well as other cognitive functions like higher executive reasoning. The temporal lobes also play a role in processing auditory information and memory encoding. While frontotemporal dementia impacts the frontal and temporal lobes, Alzheimer’s disease impacts many brain regions starting with the hippocampus and the entorhinal cortex that are essential for memory and learning. For Alzheimer’s patients, issues with memory are a hallmark sign at the beginning of the disease process, but frontotemporal dementia can look similar to Alzheimer’s nonetheless. Early on, frontotemporal dementia tends to impact personality, behavior, and language rather than memory, but in clinical practice, doctors often have a hard time differentiating between Alzheimer’s memory issues and frontotemporal language and verbal articulation issues.
One of the most striking differences between Alzheimer’s and frontotemporal dementia in terms of how these two disease processes are differentiated diagnostically has to do with age. While Alzheimer’s is typically only diagnosed after age 65, frontotemporal dementia can be diagnosed when a patient is only 40 years old. At this young age, frontotemporal dementia is a devastating, terminal diagnosis. There are reasons why it might be helpful to know that neurodegenerative processes underlie strange neurological symptoms, but dementia is a term that suggests a very bleak treatment path leading directly to long-term care.
A bleak, hopeless diagnosis can sometimes cause patients to step back from conventional medicine and consider other treatment options and other ways of viewing dementia and neurodegeneration in general.
The boundary between Lewy body dementia and Parkinson’s disease is not clear cut even if high-tech PET or SPECT diagnostics claim to tell the difference. While researching Parkinson’s disease in the early 1900’s, Friederich, H. Lewy discovered abnormal protein deposits that disrupt the functioning of the brain. When these proteins are found in the substantia nigra of the brain stem, they deplete dopamine and cause symptoms of Parkinson’s disease like tremors and movement disorder. But when these Lewy bodies (proteins) are found in other areas of the brain, they deplete acetylcholine levels which causes disturbances in how the patient perceives the world, behaves, and thinks. These two diseases share many symptoms and clinical features including Lewy bodies. Indeed, if the patient first presents with the symptoms of dementia, the diagnosis is Dementia with Lewy Bodies (DLB or LBD). Patients who are diagnosed with this form of dementia often develop many of the clinical symptoms of Parkinson’s disease eventually. On the other hand, if the patient first develops tremors and other classic symptoms and clinical features associated with Parkinson’s disease, the diagnosis is Parkinson’s.
But someone with Lewy body dementia might also be misdiagnosed with Alzheimer’s disease depending on subjective reports and the attending doctor’s perception of the problem. Older doctors may have one way of viewing a patient’s symptoms while younger doctors may tend to diagnose patients through a very different lens. A complicating fact is that PD is a disease that seems to have changed over the course of time. About 50 years ago, patients who were diagnosed with Parkinson’s disease had about a 3% chance of developing dementia. Today, the odds of developing dementia after getting diagnosed with Parkinson’s is much higher at 78%. This fact indicates that something has changed in terms of nutrition, the environment, prescription drug exposure, or another unknown (or hidden) variable over the past 50 years that has had quite an impact on the progression of Parkinson’s disease.
It’s important to note that the moment a patient arrives at a clinic for diagnosis could literally change the patient’s diagnosis.
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Age-ism in Dementia Diagnoses
Let’s consider vascular dementia. Vascular dementia happens as a result of damaged or blocked blood vessels that restrict blood flow to the brain, ultimately starving the brain of oxygen and nutrients. While Alzheimer’s (a disease involving amyloid plaques as opposed to a hypoxic brain) begins with memory loss, vascular dementia typically begins with slowed thinking, confusion, and difficulty making decisions. But any issue in the brain that involves dopamine is going to look like difficulty making decisions. And let’s face it…some people ruminate for years before making relatively simple decisions while other people are impulsive in their decision-making strategy. Doing a differential diagnosis to tease vascular dementia symptoms apart from Alzheimer’s symptoms is a lot more difficult in practice than most patients realize.
But now, just for fun, let’s think about diagnoses that are given to younger people who have similar neurological issues. In young people, poor decision making on one’s own behalf often involves addiction in terms of drugs, behaviors, or toxic relationships. We don’t diagnose young people who have poor decision-making with dementia. We diagnose them with depression, anxiety, psychosis or any number of “young-person mental health issues”. A younger individual who develops memory issues might be diagnosed with dissociative identity disorder / DID (once known as multiple personality disorder), for example while someone over the age of 40 years might receive a diagnosis of frontotemporal dementia. Lydi and I acknowledge that the presentation of a young person’s diseased state can be radically different on the surface, but we also acknowledge that underneath it all, these diagnostic labels for aging individuals are perhaps designed to funnel them into long-term care through a particular drug-administration strategy.
While a young person might be given a “chemical-restraint” drug that keeps their behavior under control, a person with dementia might be given drugs that reduce movement-related issues, but that set the patient up for an eventual, fast decline that will land them in a convalescent home. Essentially, in conventional medicine at this particular moment in time, the various “dementia” diagnoses are opportunistic. Though conventional medicine presents itself through marketing as a source of salvation for patients, in fact, there are a large number of diagnoses right now that put patients immediately on a hopeless path toward diminished quality of life and eventual death. Why has modern medicine given up on certain patients without a second thought? This is the system of medicine that has the most funding on the planet for research yet patients who want to find a hopeful prognosis must seek out ancient, low-tech models of medicine.
Frontotemporal dementia is a relatively new diagnostic label that didn’t show up until 1994. That was the time period when I (Jennifer) was working in long-term care facilities. But even after 5 years of working in long-term care from 1993 through 1998, I never heard “frontotemporal dementia” as a diagnosis for one of my patients. I also never encountered Lewy body dementia. I worked in a big city and I was an agency-worker which meant that I went to any one of up to 20 different facilities on any given day. I was exposed to a lot of patients. I worked on many Alzheimer’s wings. And I took care of a lot of younger-than-usual patients with Parkinson’s disease, but patients were often given the diagnosis “organic dementia” or “vascular dementia” when their behaviors didn’t fit what insurance companies required in order for them to receive an Alzheimer’s or Parkinson’s diagnosis. Frontotemporal dementia is a disorder that’s given to middle-aged patients who are between 45 to 64 years. Frontotemporal dementia involves personality and behavior changes and issues with language skills rather than early memory loss. But again, one has to wonder why we’re using the word “dementia” to diagnose these relatively young patients. How is it that one patient is diagnosed with frontotemporal dementia while another is diagnosed with psychosis? One of the defining criteria for frontotemporal dementia is age. Psychosis and schizophrenia is diagnosed when it takes shape in a younger patient and that’s fine, but why not label frontotemporal dementia as “frontotemporal psychosis” instead? When we tag the “frontotemporal” with “dementia” we’re suggesting long-term care as an option to loved ones. It’s a grim suggestion. And even if high-tech instruments detect neurodegeneration in the brain, are we absolutely certain that every patient with behavioral issues does not also have neurodegeneration that perhaps can heal with proper treatment? Not every psychiatric patient ends up with an MRI, after all.
“Psychosis” as a label, in contrast to dementia, suggests a mental health facility or some kind of home care. I find that it’s hard to disentangle these labels from the subtle suggestion for “treatment” that they embody. The word “psychosis” has more hope attached to it than “dementia” and I suppose that’s purposeful. If you’re trying to figure out how to overcome frontotemporal dementia, I would definitely recommend that you don’t focus on the word “dementia” and instead simply look at the neurological symptoms without any kind of age-ism clouding up your lens.
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The Evolution of Dementia
Parkinson’s disease progression has changed over the past 50 years and that’s important. Why? Because if the disease progression has changed, there has to be a reason why. If we can study the ways in which life has changed over the past 50 years, we may be able to come up with environmental changes or changes in the patient’s life that may underlie the dementia symptoms.
For example, “screen time” is a phrase that didn’t even exist 50 years ago. Fifty years ago, in my home, there was one screen: the TV. It was in the living room. We had just one heavy TV and screen time was limited because there were things to do beyond the living room. This is a major change that’s taken shape over the past 50 years, but there are other major changes that are important too.
Also, it’s important to note that infectious diseases have also changed over the course of time. For example, back in the early 1600s, patients with a Streptococcus pyogenes infection might develop scarlet fever and then later, perhaps Sydenham’s chorea (also known as the St. Vitus dance). Scarlet fever involved a rash and it could lead to heart problems and later, a movement disorder that looked similar to ADHD in children. But today, instead of scarlet fever, strep throat is the basic symptom picture for a Streptococcus pyogenes infection. Nonetheless though, even 400 years ago, a strep infection could lead to movement-related disorders because Streptococcus pyogenes is able to do molecular mimicry. In molecular mimicry a pathogen that makes itself look like human molecules and structures for the sake of camouflaging itself.
A Streptococcus pyogenes bacteria, in other words, might make itself look like human muscle tissue, specifically myosin. It might pair up with a pathogen like the Coxsackievirus which takes the shape of human muscular actin. Myosin and actin work together to produce muscle movements, but if you have pathogens inside your body that are doing molecular mimicry, you may not be able to fully control your muscle movements. Both Streptococcus pyogenes and Coxsackievirus, after all, are trying to steal your iron and if your blood is no longer a resource for them, they may try to take up residency in your muscle tissues and hide out using this molecular mimicry strategy to remain hidden from the immune system.
There is evidence that Parkinson’s disease may be caused by infection. In PD patients, the presence of Lewy bodies outside of the central nervous system (the brain) in areas that are in direct contact with the external environment such as the olfactory bulbs in the nose or the enteric system / the intestines has led some scientists to speculate that molecular mimicry may be the underlying cause of PD. The ability of alpha-synuclein to propagate in a prion-like manner supports the theory that the gut flora plays a causative role in PD as well as other forms of dementia.
In molecular mimicry, a pathogen of animal or plant origin might mimic nucleotide sequences of microRNAs to influence the protein expression. In dementia, transmissible, self-propagating prion-like proteins form seemingly for no known reason.
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Dementia Theories and Treatments That Actually Work
For decades, conventional medicine has focused on trying to clear amyloid-beta plaques from the brain in patients with Alzheimer’s disease, but this approach has failed time and time again. This has led some scientists to consider the idea of molecular mimicry. Indeed, the idea of endogenous retroviruses that are latent in our own DNA and released in response to metabolic stress that begins in the gut is an idea that further supports this theory of molecular mimicry. A patient may be exposed as some point in their lives to a pathogen that colonizes the body for many years. The patient may have initially gotten sick with an “infection” that seemed to “clear” after taking antibiotics, but in fact, the underlying pathogen that caused the infection may have taken up residency in some area of the body such as the liver, gallbladder, or pancreas or any number of other sites to produce low-level illness that went unnoticed for a period of time. The pathogen may be triggered to come out of hiding as a result of poor diet, high stress, or trauma to replicate and evolve into forms that can evade the immune system. But also, the pathogenic infection might initially come from within us. A pathogen, particularly retroviruses, can be encoded into our genome and their production may be be triggered inside our our own cells in response to biological or psychological-emotional stressors. These endogenous retroviruses that cause dementia symptoms may be able to use molecular mimicry to evade immune system detection.
The classical hypotheses around Alzheimer’s pathology and mechanisms of disease progression include:
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Amyloid plaques
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Tau pathology
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Neuroinflammation
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Oxidative stress
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Cellular senescence
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Endoplasmic reticulum stress
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Ubiquitin-proteasome system dysfunction
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Cholinergic dysfunction
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Glutamate excitotoxicity
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Disruption of microbiota-gut-brain axis
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Autophagy
None of these theories have yielded effective treatments in conventional medicine for Alzheimer’s disease specifically, but also for other types of dementia too. Yet there are treatments that can delay the progression of Alzheimer’s in animal models of disease. Dimethyl sulfoxide (DMSO) combined with the drug Fenobam delays Alzheimer’s progression in C. elegans suggesting that other DMSO-drug combinations might also be effective. In infected hamsters, DMSO reduced accumulation of prion-like proteins to inhibit aggregation again demonstrating the potential that this non-toxic, overt-the-counter medicine has in the treatment neurodegenerative disease. DMSO has been used in humans to successfully treat peripheral amyloidosis diseases as well. Studies indicate that DMSO by itself may not be enough to cure a prion disease like Alzheimer’s, but this drug is able to combine fluently with a number of other medications to potentiate them and take them directly where they’re needed in the body. Drug-potentiation is one of the medicinal effects of DMSO, so DMSO in combination with other medications both natural and synthetic has a lot of potential in the treatment of Alzheimer’s, Creutzfeldt-Jakob syndrome, as well as other forms of dementia, not just dementias that involve prion-like proteins.
DMSO is a medicine that requires a bit of learning to use it correctly and effectively and it should not be blindly combined with other medications without finding dosing guidelines and information stating that the drug-DMSO combination is safe, but studies indicate that this medicine is a promising agent for dementia treatment. The DMSO Guidebook was written for people who would like to learn how to use this medicine properly at home.
So while conventional medicine does not use medicines that actually work to treat dementia even though a medication like DMSO is FDA approved, this medication in particular, does show a lot of promise in at least slowing down the progression of dementia. DMSO has a healing effect on the nervous system in general so it isn’t surprising that it would have beneficial effects against dementia too, not just Alzheimer’s. DMSO has a long and truly amazing track record at healing nervous system injuries and diseases, but funding is simply not widely available to study it in terms of its effects on dementia. So, as doctors and scientists run around trying to use the most popular theories around dementia in order to find treatments, a potentially effective treatment, DMSO, is in a blind-spot.
There are, of course, other treatments for dementia and neurodegenerative disease that we’ll be expanding on in other discussions, but the main point that we wanted to express here is the idea that though conventional medicine claims to not be able to overcome dementia, scientific studies have shown that there’s still hope. DMSO is just one of several known treatments that have the ability to slow the progression of neurodegeneration or stop the progression altogether.
Other issues that may play a contributing role in terms of dementia in the developed world include nutrition and toxin exposure. Nutrition has changed dramatically in the past fifty years. Some of these important and possibly relevant changes include:
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The end of iodine fortification of bread. Instead iodine is now added to salt, a poor carrier for iodine. A deficiency of iodine can cause cancer and lead to other health problems.
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The addition of bromine to all commercial bread products as well as to soft drinks (especially citrus drinks like Mountain Dew and Gatorade). Bromine competes with iodine in the body and has a negative impact on the brain and nervous system.
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The hybridization and genetic modification of fruits to exclude seeds. Seeds contain vitamin B17 (also known as laetrile or amygdalin) a medicinal substance that prevents and treats cancer.
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The criminalization of vitamin B17. It is illegal to buy or sell vitamin B17 supplements in the United States because this vitamin has been shown to prevent and in some cases cure all degenerative diseases including cancer. Many Americans eat apricot kernels (20-40 per day throughout the day-not all at once- usually 5 kernels which should be eaten only on an empty stomach. If they’re mixed with food, they become less potent).
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Inaccessibility of Vitamin B12. Vitamin B12 should be administered as an injection or it should be combined with DMSO (to ensure that it is properly absorbed) and administered either topically or orally. Vitamin B12 supplements by themselves that are taken by mouth are often ineffective. Symptoms of vitamin B12 deficiency are similar to and/or mimic symptoms of dementia.
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Choline and Phosphatidylcholine - Choline is a precursor of phosphatidylcholine and acetylcholine. Acetylcholine plays a role in many neurodegenerative diseases.
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Other important changes that might be relevant to the development of dementia:
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Adding bromine to swimming pools instead of chlorine for water purification. Symptoms of bromine intoxication mimic and include symptoms of dementia. Bromine builds up in the body over time.
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The use of bromine as a fire retardant in furnishings and pajamas as well as vehicle interiors.
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While mercury amalgam fillings are not used in most of the world, the U.S. has continued to endorse the use of amalgam for dental fillings. Mercury and other heavy metals have been implicated by many studies as a possible cause of various types of dementia.
I
Final Considerations
If you or a loved one has recently received a “dementia-diagnosis”, it can be helpful to take a step back from the details and consider diagnoses that might be applied to younger individuals. I’m not suggesting that amyloid plaques are not an underlying cause of Alzheimer’s or that Parkinson’s disease is not caused by dopamine-receptor issues. Rather, I’m suggesting that we need to consider how doctors are trained to diagnose patients with dementia on the basis of their age and how this strategy can be harmful. A diagnosis of dementia is always aiming toward long-term care as a final destination which should make readers question whether they should even adopt this diagnosis and take ownership of it psychologically. If you are looking for a cure for a neurological disorder that’s been diagnosed as “dementia”, a good starting block would be to step away from the word “dementia” and instead, look for treatments outside of conventional medicine to prevent and reverse symptoms.
Exposure to toxins, poor nutrition, and trauma can all play a role in the development of dementia but there are ways to reverse some of the damage done by toxin exposure in some cases. Also, there are treatments that are available for dementia, but they haven’t necessarily been studied as extensively as treatments that fit neatly into the model that’s been propagated by Big Pharma. Big Pharma funds models of medicine that are seriously flawed at times in order to prevent scientists from looking too closely at the treatments that may actually work, but that either don’t fit the model or that haven’t been funded well enough to prove their effectiveness.
Dementia is a serious illness, but patients who don’t start taking prescription medications as a result of diagnosis can begin working right away with medicines like high-dose DMSO at home along with other treatments that combine well with DMSO for dementia.
Though, as a culture, we’ve had an opportunity to look at millions, if not billions of MRIs, CTs, X-rays, PET Scans, etc. of the brain and body, most of these scans do not look at normal, healthy people’s brains. Recently, doctors have been required by insurance companies to do early diagnostics on patients with possible dementia. This has led to the observation that patients with the following health issues may be identified as early dementia patients even though their symptoms are totally reversible:
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Depression
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Adverse drug effects
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Drug addiction
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Alcohol addiction
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Surgical brain lesions
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Normal pressure hydrocephalus
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Space-occupying nervous system lesions
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Metabolic disorders
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Hypothyroidism
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Hypoparathyroidism
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Vitamin B12 deficiency
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Central nervous system infection
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Neurosyphilis
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HIV
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When I look at this list in light of new research exploring issues like endogenous retroviruses and molecular mimicry, it seems like this list should probably be a lot longer. Most doctors don’t test patients for neurosyphilis even though, in homeopathy, syphilis is a miasm, which means that it is, in some cases, an endogenous retroviruses that arises from inside of us versus through exposure from the external environment. The syphilis miasm (syphilinism) is a core predisposition in some patients that arises from the ancestry to produce destruction, decay, and distortion.
The idea here is to consider the idea that there are reversible dementias that don’t fit the model presented in conventional medicine and scientific research. And there are medicines and treatments that are not being used in conventional medicine that slow or halt the progression of dementia. Though some doctors may be very interested in these kinds of ideas and they may even wish that they could prescribe medicines like DMSO to their dementia patients, doctors have rules that they have to follow in order to maintain their licenses. And Big Pharma is cruel to doctors that try to buck the system. This is why there’s a huge disconnect between what doctors present to their dementia patients and what actually exists in the world, not just in conventional medicine, to treat dementia. Doctors are not allowed to be creative with patients except within very clearly delineated limits.
Resources
Olthof, M. R., Brink, E. J., Katan, M. B., Verhoef, P. (2005). Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men. Retrieved June 22, 2019 from https://academic.oup.com/ajcn/article/82/1/111/4863306
Wood, J. L., Allison, R. G. (1982). Effects of consumption of choline and lecithin on neurological and cardiovascular systems. Retrieved June 22, 2019 from https://www.ncbi.nlm.nih.gov/pubmed/6754453
Dr. Axe (2019). What is choline? Retrieved June 22, 2019 from https://draxe.com/what-is-choline/
Griffin, G. E. (1974). World Without Cancer, 3rd Ed. American Media Inc.
Barbeau, A. (1978). Emerging treatments: replacement therapy with choline or lecithin in neurological diseases. Retrieved June 22, 2019 from https://www.ncbi.nlm.nih.gov/pubmed/148319
Altoida (2022). How Is Frontotemporal Dementia Different from Alzheimer’s? Retrieved July 1, 2026 from https://altoida.com/blog/frontotemporal-dementia-different-from-alzheimers/
Miraglia, F. and Colla, E. (2019). Microbiome, Parkinson’s Disease, and Molecular Mimicry. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/30866550/
Friedland, R. P. (2015). Mechanisms of molecular mimicry involving the microbiota in neurodegeneration. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/25589730/
Abuhassan, Q. et al. (2026). Viral Mimicry of Alzheimer’s Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/42071158/
Ivanova, A. V. et al. (2025). Alzheimer’s Disease: From Molecular Mechanisms to Promising Therapeutic Strategies. Retrieved July 1, 2026 from https://www.mdpi.com/1422-0067/26/19/9444
Sadananada, G. et al. (2021). DMSO Delays Alzheimer Disease Causing AB-induced Paralysis in C. elegans Through Modulation of Glutamate/Acetylcholine Neurotransmission. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC8558977/
Penazzi, L. et al. (2016). DMSO modulates CNS function in a preclinical Alzheimer’s disease model. Retrieved July 1, 2026 from https://www.sciencedirect.com/science/article/pii/S0028390816304749
Shaked, G. and Engelstein, R. (2003). Dimethyl sulfoxide delays PrPsc accumulation and disease symptoms in prion-infected hamsters. Retrieved July 1, 2026 from https://www.sciencedirect.com/science/article/abs/pii/S0006899303030452
Barret, A. et al. (2003). Evaluation of Quinacrine Treatment for Prion Diseases. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC165262/
Murakami-Kubo, I. et al. (2004). Quinoline derivatives are therapeutic candidates for transmissible spongiform encephalopathies. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/14722283/
Hashmi, M. U. (2023). Exploring Methylene Blue and Its Derivatives in Alzheimer’s Treatment: A Comprehensive Review of Randomized Control Trials. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC10631450/
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How Parkinson's Dementia and Lewy Body Dementia Are Related Diseases
Dementia is not technically a diagnosis in conventional medicine. Rather, it’s a term that’s used to describe a set of symptoms that involve the following:
-
Memory decline
-
Reasoning decline
-
Difficulty thinking
-
Difficulty performing other cognitive functions
In order to diagnose a patient with a type of dementia, there must be memory problems and at least one other issue affecting the patient’s cognition such as language disturbances, movement issues, failure to recognize familiar objects, and disturbances in planning, organizing, sequencing, or abstracting information. These deficits in memory and cognition must interfere with the patient’s occupational and social function. There must also be some kind of evidence of systemic health problems or a brain disorder as the primary underlying cause of the cognitive deficits using through diagnostic neuroimaging tests.
Neuroimaging is a standard part of the protocol for doctors in developed nations of the world to detect conditions like subdural hematomas, cerebral infarcts or tumors, and normal pressure hydrocephalus that can produce symptoms similar to dementia. Lab work should also be done to determine if the patient has depression, vitamin B12 deficiency, or hypothyroidism because these issues also look and seem like dementia in terms of signs and symptoms.
In fact, studies have reported that the frequency of reversible dementias among patients who are diagnosed with an irreversible type of dementia is between 0 to 23%. So below, we’ll talk about dementia in conventional medicine and reasons why you should question a diagnosis of dementia and seek out alternative treatments that may be more effective than what the doctor is prescribing.
In a previous article about disease family trees, we talked about how it could be difficult to find information about Lewy body dementia research cure options, but how you could look instead for research talking about a Parkinson's disease cure instead because these two types of dementia share many things in common. But Parkinson’s and Lewy body dementia are not the only types of dementia that can be hard to differentiate using only symptom comparison without high-tech equipment.
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Alzheimer’s disease tends to begin with memory issues while Lewy body dementia starts with hallucinations. Parkinson’s may begin with movement related symptoms first which makes it stand out a bit from Lewy body dementia and Alzheimer’s, though in practice, it might not be easy to determine which is which.
Parkinson’s disease is caused by the loss of dopamine-producing neurons in the substantia nigra. The substantia nigra is a part of the brain that plays a critical role in reward and movement. Lewy body dementia shares a number of clinical, neuropsychological, and pathological features with Parkinson’s disease, but it involves more than one part of the brain and more than one type of cell (dopaminergic and cholinergic cells). The differences between Parkinson’s disease and Lewy body dementia (and between Lewy body dementia or Parkinson’s and Alzheimer’s) is important if you are seeking stem cell treatment, for example. Stem cells work best when the treatment is very targeted within a discreet area on just one type of cell. But other types of treatments for dementia have a more holistic effect on nervous system healing. For this reason, it isn’t always essential to have access to high-tech diagnostic equipment or to receive a very definitive diagnosis in order to get started treating neurodegenerative disease symptoms.
Scientists who study neurodegenerative disorders have noted that correctly diagnosing “dementia with Lewy bodies / DLB” is challenging and many patients who show symptoms of this disease are misdiagnosed as having Parkinson’s. What’s the point of differentiating between two diseases that are so similar? If doctors can’t tell the difference between PD and LBD, why are they regarded as different diseases?
One-Pill-for-One-Disease
The answer to that question has to do, in part, with the One-Pill-for-One-Disease paradigm that Big Pharma developed many years ago as a way to market conventional medicine. As a result of the marketing that’s been done over the years, there is a quiet, unspoken belief that, when you go to the doctor, he or she will be able to prescribe a pill, just one pill, that you will take to overcome your diseased state. Indeed, this idea of One-Pill-for-One-Disease, has been propagated in part by combining drugs into one pill when two or more drugs are normally prescribed together by doctors. Of course, simplicity can be beneficial. Patients don’t always follow their doctor’s orders even when there is only one pill involved in their treatment. But the idea here is that, if there is only One-Pill-for-One-Disease, you have to have a lot of different diseases – or rather, a lot of different diagnostic labels in order to ensure that patients receive a drug that targets the specific presentation of disease that’s manifesting in their body.
Unfortunately though, this One-Pill-for-One-Disease paradigm is often more about making profit than about finding the perfect drug to fit a particular disease. The One-Pill-for-One-Disease idea was meant to simplify medicine, but often, it creates a muddled mess. For example, is Lewy body dementia actually different from Parkinson’s disease or are these two diseases actually made up of the same underlying physical issues? The One-Pill-for-One-Disease also really hijacks the reality that sick people often need lifestyle and diet changes that involve something much more involved than just taking one pill.
Different Types of Dementia
The gold standard for diagnosing dementia with Lewy bodies is a PET scan and single-photo emission computed tomography (SPECT) tracers. Dopamine transporter loss in the brain is the signature feature of LBD in conventional medicine. As LBD progresses, it impacts a bigger area of the brain than PD, though in Alzheimer’s, brain damage can impact a larger area similar to what’s observed in LBD. The loss of dopamine transporters in LBD helps to differentiate this disease from other types of dementia such as Alzheimer’s, but Alzheimer's is a neurodegenerative brain disorder that mostly impacts memory and language. In contrast, PD tends to impact movement and coordination while LBD involves hallucinations and REM sleep disorder. Alzheimer’s begins with memory loss, but Parkinson’s patients typically complain about physical stiffness and tremors as their first set of symptoms. LBD patients begin with symptoms that resemble Alzheimer’s, but the disease progresses more in the direction of eventual Parkinson’s symptoms. Alzheimer’s patients, in contrast, are unlikely to eventually develop movement-related issues.
Frontotemporal dementia and Alzheimer’s disease are similar, but they affect different regions of the brain. Frontotemporal dementia, as the name suggests, impacts the front of the brain including the frontal and the temporal lobes. These areas of the brain are associated with personality, behavior, and language, as well as other cognitive functions like higher executive reasoning. The temporal lobes also play a role in processing auditory information and memory encoding. While frontotemporal dementia impacts the frontal and temporal lobes, Alzheimer’s disease impacts many brain regions starting with the hippocampus and the entorhinal cortex that are essential for memory and learning. For Alzheimer’s patients, issues with memory are a hallmark sign at the beginning of the disease process, but frontotemporal dementia can look similar to Alzheimer’s nonetheless. Early on, frontotemporal dementia tends to impact personality, behavior, and language rather than memory, but in clinical practice, doctors often have a hard time differentiating between Alzheimer’s memory issues and frontotemporal language and verbal articulation issues.
One of the most striking differences between Alzheimer’s and frontotemporal dementia in terms of how these two disease processes are differentiated diagnostically has to do with age. While Alzheimer’s is typically only diagnosed after age 65, frontotemporal dementia can be diagnosed when a patient is only 40 years old. At this young age, frontotemporal dementia is a devastating, terminal diagnosis. There are reasons why it might be helpful to know that neurodegenerative processes underlie strange neurological symptoms, but dementia is a term that suggests a very bleak treatment path leading directly to long-term care.
A bleak, hopeless diagnosis can sometimes cause patients to step back from conventional medicine and consider other treatment options and other ways of viewing dementia and neurodegeneration in general.
The boundary between Lewy body dementia and Parkinson’s disease is not clear cut even if high-tech PET or SPECT diagnostics claim to tell the difference. While researching Parkinson’s disease in the early 1900’s, Friederich, H. Lewy discovered abnormal protein deposits that disrupt the functioning of the brain. When these proteins are found in the substantia nigra of the brain stem, they deplete dopamine and cause symptoms of Parkinson’s disease like tremors and movement disorder. But when these Lewy bodies (proteins) are found in other areas of the brain, they deplete acetylcholine levels which causes disturbances in how the patient perceives the world, behaves, and thinks. These two diseases share many symptoms and clinical features including Lewy bodies. Indeed, if the patient first presents with the symptoms of dementia, the diagnosis is Dementia with Lewy Bodies (DLB or LBD). Patients who are diagnosed with this form of dementia often develop many of the clinical symptoms of Parkinson’s disease eventually. On the other hand, if the patient first develops tremors and other classic symptoms and clinical features associated with Parkinson’s disease, the diagnosis is Parkinson’s.
But someone with Lewy body dementia might also be misdiagnosed with Alzheimer’s disease depending on subjective reports and the attending doctor’s perception of the problem. Older doctors may have one way of viewing a patient’s symptoms while younger doctors may tend to diagnose patients through a very different lens. A complicating fact is that PD is a disease that seems to have changed over the course of time. About 50 years ago, patients who were diagnosed with Parkinson’s disease had about a 3% chance of developing dementia. Today, the odds of developing dementia after getting diagnosed with Parkinson’s is much higher at 78%. This fact indicates that something has changed in terms of nutrition, the environment, prescription drug exposure, or another unknown (or hidden) variable over the past 50 years that has had quite an impact on the progression of Parkinson’s disease.
It’s important to note that the moment a patient arrives at a clinic for diagnosis could literally change the patient’s diagnosis.
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Age-ism in Dementia Diagnoses
Let’s consider vascular dementia. Vascular dementia happens as a result of damaged or blocked blood vessels that restrict blood flow to the brain, ultimately starving the brain of oxygen and nutrients. While Alzheimer’s (a disease involving amyloid plaques as opposed to a hypoxic brain) begins with memory loss, vascular dementia typically begins with slowed thinking, confusion, and difficulty making decisions. But any issue in the brain that involves dopamine is going to look like difficulty making decisions. And let’s face it…some people ruminate for years before making relatively simple decisions while other people are impulsive in their decision-making strategy. Doing a differential diagnosis to tease vascular dementia symptoms apart from Alzheimer’s symptoms is a lot more difficult in practice than most patients realize.
But now, just for fun, let’s think about diagnoses that are given to younger people who have similar neurological issues. In young people, poor decision making on one’s own behalf often involves addiction in terms of drugs, behaviors, or toxic relationships. We don’t diagnose young people who have poor decision-making with dementia. We diagnose them with depression, anxiety, psychosis or any number of “young-person mental health issues”. A younger individual who develops memory issues might be diagnosed with dissociative identity disorder / DID (once known as multiple personality disorder), for example while someone over the age of 40 years might receive a diagnosis of frontotemporal dementia. Lydi and I acknowledge that the presentation of a young person’s diseased state can be radically different on the surface, but we also acknowledge that underneath it all, these diagnostic labels for aging individuals are perhaps designed to funnel them into long-term care through a particular drug-administration strategy.
While a young person might be given a “chemical-restraint” drug that keeps their behavior under control, a person with dementia might be given drugs that reduce movement-related issues, but that set the patient up for an eventual, fast decline that will land them in a convalescent home. Essentially, in conventional medicine at this particular moment in time, the various “dementia” diagnoses are opportunistic. Though conventional medicine presents itself through marketing as a source of salvation for patients, in fact, there are a large number of diagnoses right now that put patients immediately on a hopeless path toward diminished quality of life and eventual death. Why has modern medicine given up on certain patients without a second thought? This is the system of medicine that has the most funding on the planet for research yet patients who want to find a hopeful prognosis must seek out ancient, low-tech models of medicine.
Frontotemporal dementia is a relatively new diagnostic label that didn’t show up until 1994. That was the time period when I (Jennifer) was working in long-term care facilities. But even after 5 years of working in long-term care from 1993 through 1998, I never heard “frontotemporal dementia” as a diagnosis for one of my patients. I also never encountered Lewy body dementia. I worked in a big city and I was an agency-worker which meant that I went to any one of up to 20 different facilities on any given day. I was exposed to a lot of patients. I worked on many Alzheimer’s wings. And I took care of a lot of younger-than-usual patients with Parkinson’s disease, but patients were often given the diagnosis “organic dementia” or “vascular dementia” when their behaviors didn’t fit what insurance companies required in order for them to receive an Alzheimer’s or Parkinson’s diagnosis. Frontotemporal dementia is a disorder that’s given to middle-aged patients who are between 45 to 64 years. Frontotemporal dementia involves personality and behavior changes and issues with language skills rather than early memory loss. But again, one has to wonder why we’re using the word “dementia” to diagnose these relatively young patients. How is it that one patient is diagnosed with frontotemporal dementia while another is diagnosed with psychosis? One of the defining criteria for frontotemporal dementia is age. Psychosis and schizophrenia is diagnosed when it takes shape in a younger patient and that’s fine, but why not label frontotemporal dementia as “frontotemporal psychosis” instead? When we tag the “frontotemporal” with “dementia” we’re suggesting long-term care as an option to loved ones. It’s a grim suggestion. And even if high-tech instruments detect neurodegeneration in the brain, are we absolutely certain that every patient with behavioral issues does not also have neurodegeneration that perhaps can heal with proper treatment? Not every psychiatric patient ends up with an MRI, after all.
“Psychosis” as a label, in contrast to dementia, suggests a mental health facility or some kind of home care. I find that it’s hard to disentangle these labels from the subtle suggestion for “treatment” that they embody. The word “psychosis” has more hope attached to it than “dementia” and I suppose that’s purposeful. If you’re trying to figure out how to overcome frontotemporal dementia, I would definitely recommend that you don’t focus on the word “dementia” and instead simply look at the neurological symptoms without any kind of age-ism clouding up your lens.
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The Evolution of Dementia
Parkinson’s disease progression has changed over the past 50 years and that’s important. Why? Because if the disease progression has changed, there has to be a reason why. If we can study the ways in which life has changed over the past 50 years, we may be able to come up with environmental changes or changes in the patient’s life that may underlie the dementia symptoms.
For example, “screen time” is a phrase that didn’t even exist 50 years ago. Fifty years ago, in my home, there was one screen: the TV. It was in the living room. We had just one heavy TV and screen time was limited because there were things to do beyond the living room. This is a major change that’s taken shape over the past 50 years, but there are other major changes that are important too.
Also, it’s important to note that infectious diseases have also changed over the course of time. For example, back in the early 1600s, patients with a Streptococcus pyogenes infection might develop scarlet fever and then later, perhaps Sydenham’s chorea (also known as the St. Vitus dance). Scarlet fever involved a rash and it could lead to heart problems and later, a movement disorder that looked similar to ADHD in children. But today, instead of scarlet fever, strep throat is the basic symptom picture for a Streptococcus pyogenes infection. Nonetheless though, even 400 years ago, a strep infection could lead to movement-related disorders because Streptococcus pyogenes is able to do molecular mimicry. In molecular mimicry a pathogen that makes itself look like human molecules and structures for the sake of camouflaging itself.
A Streptococcus pyogenes bacteria, in other words, might make itself look like human muscle tissue, specifically myosin. It might pair up with a pathogen like the Coxsackievirus which takes the shape of human muscular actin. Myosin and actin work together to produce muscle movements, but if you have pathogens inside your body that are doing molecular mimicry, you may not be able to fully control your muscle movements. Both Streptococcus pyogenes and Coxsackievirus, after all, are trying to steal your iron and if your blood is no longer a resource for them, they may try to take up residency in your muscle tissues and hide out using this molecular mimicry strategy to remain hidden from the immune system.
There is evidence that Parkinson’s disease may be caused by infection. In PD patients, the presence of Lewy bodies outside of the central nervous system (the brain) in areas that are in direct contact with the external environment such as the olfactory bulbs in the nose or the enteric system / the intestines has led some scientists to speculate that molecular mimicry may be the underlying cause of PD. The ability of alpha-synuclein to propagate in a prion-like manner supports the theory that the gut flora plays a causative role in PD as well as other forms of dementia.
In molecular mimicry, a pathogen of animal or plant origin might mimic nucleotide sequences of microRNAs to influence the protein expression. In dementia, transmissible, self-propagating prion-like proteins form seemingly for no known reason.
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Dementia Theories and Treatments That Actually Work
For decades, conventional medicine has focused on trying to clear amyloid-beta plaques from the brain in patients with Alzheimer’s disease, but this approach has failed time and time again. This has led some scientists to consider the idea of molecular mimicry. Indeed, the idea of endogenous retroviruses that are latent in our own DNA and released in response to metabolic stress that begins in the gut is an idea that further supports this theory of molecular mimicry. A patient may be exposed as some point in their lives to a pathogen that colonizes the body for many years. The patient may have initially gotten sick with an “infection” that seemed to “clear” after taking antibiotics, but in fact, the underlying pathogen that caused the infection may have taken up residency in some area of the body such as the liver, gallbladder, or pancreas or any number of other sites to produce low-level illness that went unnoticed for a period of time. The pathogen may be triggered to come out of hiding as a result of poor diet, high stress, or trauma to replicate and evolve into forms that can evade the immune system. But also, the pathogenic infection might initially come from within us. A pathogen, particularly retroviruses, can be encoded into our genome and their production may be be triggered inside our our own cells in response to biological or psychological-emotional stressors. These endogenous retroviruses that cause dementia symptoms may be able to use molecular mimicry to evade immune system detection.
The classical hypotheses around Alzheimer’s pathology and mechanisms of disease progression include:
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Amyloid plaques
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Tau pathology
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Neuroinflammation
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Oxidative stress
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Cellular senescence
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Endoplasmic reticulum stress
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Ubiquitin-proteasome system dysfunction
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Cholinergic dysfunction
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Glutamate excitotoxicity
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Disruption of microbiota-gut-brain axis
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Autophagy
None of these theories have yielded effective treatments in conventional medicine for Alzheimer’s disease specifically, but also for other types of dementia too. Yet there are treatments that can delay the progression of Alzheimer’s in animal models of disease. Dimethyl sulfoxide (DMSO) combined with the drug Fenobam delays Alzheimer’s progression in C. elegans suggesting that other DMSO-drug combinations might also be effective. In infected hamsters, DMSO reduced accumulation of prion-like proteins to inhibit aggregation again demonstrating the potential that this non-toxic, overt-the-counter medicine has in the treatment neurodegenerative disease. DMSO has been used in humans to successfully treat peripheral amyloidosis diseases as well. Studies indicate that DMSO by itself may not be enough to cure a prion disease like Alzheimer’s, but this drug is able to combine fluently with a number of other medications to potentiate them and take them directly where they’re needed in the body. Drug-potentiation is one of the medicinal effects of DMSO, so DMSO in combination with other medications both natural and synthetic has a lot of potential in the treatment of Alzheimer’s, Creutzfeldt-Jakob syndrome, as well as other forms of dementia, not just dementias that involve prion-like proteins.
DMSO is a medicine that requires a bit of learning to use it correctly and effectively and it should not be blindly combined with other medications without finding dosing guidelines and information stating that the drug-DMSO combination is safe, but studies indicate that this medicine is a promising agent for dementia treatment. The DMSO Guidebook was written for people who would like to learn how to use this medicine properly at home.
So while conventional medicine does not use medicines that actually work to treat dementia even though a medication like DMSO is FDA approved, this medication in particular, does show a lot of promise in at least slowing down the progression of dementia. DMSO has a healing effect on the nervous system in general so it isn’t surprising that it would have beneficial effects against dementia too, not just Alzheimer’s. DMSO has a long and truly amazing track record at healing nervous system injuries and diseases, but funding is simply not widely available to study it in terms of its effects on dementia. So, as doctors and scientists run around trying to use the most popular theories around dementia in order to find treatments, a potentially effective treatment, DMSO, is in a blind-spot.
There are, of course, other treatments for dementia and neurodegenerative disease that we’ll be expanding on in other discussions, but the main point that we wanted to express here is the idea that though conventional medicine claims to not be able to overcome dementia, scientific studies have shown that there’s still hope. DMSO is just one of several known treatments that have the ability to slow the progression of neurodegeneration or stop the progression altogether.
Other issues that may play a contributing role in terms of dementia in the developed world include nutrition and toxin exposure. Nutrition has changed dramatically in the past fifty years. Some of these important and possibly relevant changes include:
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The end of iodine fortification of bread. Instead iodine is now added to salt, a poor carrier for iodine. A deficiency of iodine can cause cancer and lead to other health problems.
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The addition of bromine to all commercial bread products as well as to soft drinks (especially citrus drinks like Mountain Dew and Gatorade). Bromine competes with iodine in the body and has a negative impact on the brain and nervous system.
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The hybridization and genetic modification of fruits to exclude seeds. Seeds contain vitamin B17 (also known as laetrile or amygdalin) a medicinal substance that prevents and treats cancer.
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The criminalization of vitamin B17. It is illegal to buy or sell vitamin B17 supplements in the United States because this vitamin has been shown to prevent and in some cases cure all degenerative diseases including cancer. Many Americans eat apricot kernels (20-40 per day throughout the day-not all at once- usually 5 kernels which should be eaten only on an empty stomach. If they’re mixed with food, they become less potent).
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Inaccessibility of Vitamin B12. Vitamin B12 should be administered as an injection or it should be combined with DMSO (to ensure that it is properly absorbed) and administered either topically or orally. Vitamin B12 supplements by themselves that are taken by mouth are often ineffective. Symptoms of vitamin B12 deficiency are similar to and/or mimic symptoms of dementia.
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Choline and Phosphatidylcholine - Choline is a precursor of phosphatidylcholine and acetylcholine. Acetylcholine plays a role in many neurodegenerative diseases.
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Other important changes that might be relevant to the development of dementia:
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Adding bromine to swimming pools instead of chlorine for water purification. Symptoms of bromine intoxication mimic and include symptoms of dementia. Bromine builds up in the body over time.
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The use of bromine as a fire retardant in furnishings and pajamas as well as vehicle interiors.
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While mercury amalgam fillings are not used in most of the world, the U.S. has continued to endorse the use of amalgam for dental fillings. Mercury and other heavy metals have been implicated by many studies as a possible cause of various types of dementia.
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Final Considerations
If you or a loved one has recently received a “dementia-diagnosis”, it can be helpful to take a step back from the details and consider diagnoses that might be applied to younger individuals. I’m not suggesting that amyloid plaques are not an underlying cause of Alzheimer’s or that Parkinson’s disease is not caused by dopamine-receptor issues. Rather, I’m suggesting that we need to consider how doctors are trained to diagnose patients with dementia on the basis of their age and how this strategy can be harmful. A diagnosis of dementia is always aiming toward long-term care as a final destination which should make readers question whether they should even adopt this diagnosis and take ownership of it psychologically. If you are looking for a cure for a neurological disorder that’s been diagnosed as “dementia”, a good starting block would be to step away from the word “dementia” and instead, look for treatments outside of conventional medicine to prevent and reverse symptoms.
Exposure to toxins, poor nutrition, and trauma can all play a role in the development of dementia but there are ways to reverse some of the damage done by toxin exposure in some cases. Also, there are treatments that are available for dementia, but they haven’t necessarily been studied as extensively as treatments that fit neatly into the model that’s been propagated by Big Pharma. Big Pharma funds models of medicine that are seriously flawed at times in order to prevent scientists from looking too closely at the treatments that may actually work, but that either don’t fit the model or that haven’t been funded well enough to prove their effectiveness.
Dementia is a serious illness, but patients who don’t start taking prescription medications as a result of diagnosis can begin working right away with medicines like high-dose DMSO at home along with other treatments that combine well with DMSO for dementia.
Though, as a culture, we’ve had an opportunity to look at millions, if not billions of MRIs, CTs, X-rays, PET Scans, etc. of the brain and body, most of these scans do not look at normal, healthy people’s brains. Recently, doctors have been required by insurance companies to do early diagnostics on patients with possible dementia. This has led to the observation that patients with the following health issues may be identified as early dementia patients even though their symptoms are totally reversible:
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Depression
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Adverse drug effects
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Drug addiction
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Alcohol addiction
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Surgical brain lesions
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Normal pressure hydrocephalus
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Space-occupying nervous system lesions
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Metabolic disorders
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Hypothyroidism
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Hypoparathyroidism
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Vitamin B12 deficiency
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Central nervous system infection
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Neurosyphilis
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HIV
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When I look at this list in light of new research exploring issues like endogenous retroviruses and molecular mimicry, it seems like this list should probably be a lot longer. Most doctors don’t test patients for neurosyphilis even though, in homeopathy, syphilis is a miasm, which means that it is, in some cases, an endogenous retroviruses that arises from inside of us versus through exposure from the external environment. The syphilis miasm (syphilinism) is a core predisposition in some patients that arises from the ancestry to produce destruction, decay, and distortion.
The idea here is to consider the idea that there are reversible dementias that don’t fit the model presented in conventional medicine and scientific research. And there are medicines and treatments that are not being used in conventional medicine that slow or halt the progression of dementia. Though some doctors may be very interested in these kinds of ideas and they may even wish that they could prescribe medicines like DMSO to their dementia patients, doctors have rules that they have to follow in order to maintain their licenses. And Big Pharma is cruel to doctors that try to buck the system. This is why there’s a huge disconnect between what doctors present to their dementia patients and what actually exists in the world, not just in conventional medicine, to treat dementia. Doctors are not allowed to be creative with patients except within very clearly delineated limits.
Resources
Olthof, M. R., Brink, E. J., Katan, M. B., Verhoef, P. (2005). Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men. Retrieved June 22, 2019 from https://academic.oup.com/ajcn/article/82/1/111/4863306
Wood, J. L., Allison, R. G. (1982). Effects of consumption of choline and lecithin on neurological and cardiovascular systems. Retrieved June 22, 2019 from https://www.ncbi.nlm.nih.gov/pubmed/6754453
Dr. Axe (2019). What is choline? Retrieved June 22, 2019 from https://draxe.com/what-is-choline/
Griffin, G. E. (1974). World Without Cancer, 3rd Ed. American Media Inc.
Barbeau, A. (1978). Emerging treatments: replacement therapy with choline or lecithin in neurological diseases. Retrieved June 22, 2019 from https://www.ncbi.nlm.nih.gov/pubmed/148319
Altoida (2022). How Is Frontotemporal Dementia Different from Alzheimer’s? Retrieved July 1, 2026 from https://altoida.com/blog/frontotemporal-dementia-different-from-alzheimers/
Miraglia, F. and Colla, E. (2019). Microbiome, Parkinson’s Disease, and Molecular Mimicry. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/30866550/
Friedland, R. P. (2015). Mechanisms of molecular mimicry involving the microbiota in neurodegeneration. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/25589730/
Abuhassan, Q. et al. (2026). Viral Mimicry of Alzheimer’s Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/42071158/
Ivanova, A. V. et al. (2025). Alzheimer’s Disease: From Molecular Mechanisms to Promising Therapeutic Strategies. Retrieved July 1, 2026 from https://www.mdpi.com/1422-0067/26/19/9444
Sadananada, G. et al. (2021). DMSO Delays Alzheimer Disease Causing AB-induced Paralysis in C. elegans Through Modulation of Glutamate/Acetylcholine Neurotransmission. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC8558977/
Penazzi, L. et al. (2016). DMSO modulates CNS function in a preclinical Alzheimer’s disease model. Retrieved July 1, 2026 from https://www.sciencedirect.com/science/article/pii/S0028390816304749
Shaked, G. and Engelstein, R. (2003). Dimethyl sulfoxide delays PrPsc accumulation and disease symptoms in prion-infected hamsters. Retrieved July 1, 2026 from https://www.sciencedirect.com/science/article/abs/pii/S0006899303030452
Barret, A. et al. (2003). Evaluation of Quinacrine Treatment for Prion Diseases. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC165262/
Murakami-Kubo, I. et al. (2004). Quinoline derivatives are therapeutic candidates for transmissible spongiform encephalopathies. Retrieved July 1, 2026 from https://pubmed.ncbi.nlm.nih.gov/14722283/
Hashmi, M. U. (2023). Exploring Methylene Blue and Its Derivatives in Alzheimer’s Treatment: A Comprehensive Review of Randomized Control Trials. Retrieved July 1, 2026 from https://pmc.ncbi.nlm.nih.gov/articles/PMC10631450/
