The overlap between Alzheimer’s Disease and Periodontal Disease is too substantial to ignore. Which is why the Curing Alzheimer’s Disease Foundation is literally paying to fully investigate if gum disease is causing Alzheimer’s. Join us through your tax deductible donation and help us See The Science Through
KNOW YOUR ALZHEIMER’S RISKS: #2 GUM DISEASE Read Post »
77% of Late Onset Alzheimer’s Disease have NO genetic connection If a genetic mutation predisposes you to Alzheimer’s, then we would see a much stronger familial link for this disease – which we don’t. What we do see is pretty shocking. Of the multiple large scale studies we reviewed, 77% of Late Onset AD cases (referred to as LOAD) have absolutely NO family history of AD! Which makes the slight (16%) of AD cases whose mother also died of the disease a bit underwhelming. Here’s the Data that will leave you sleeping better at night A review of 3,342 confirmed AD cases shows: *No Family History represented 77% of the cases *Having a mother with AD represented 16% of the cases *Having a father with AD represented 6% of the cases Yet many researchers suspect Alzheimer’s is genetic? When we look at Alzheimer’s Disease from genes as being the driver, this disease can be classified in one of two ways: Early Onset – which has certain genes linked to it including: Amyloid Precurser Protein (APP) which is located on chromosome 21; Presenilin 1 (PSEN1) which is located on chromosome 14; Presenilin 2 (PSEN2) which is located on chromosome 14 Late Onset – which has not been determined to have a definitive (though suspected) link. The only gene, which is a natural mutation, is the APOE gene. More on that in a later post Different from early onset (EOAD), which we can link directly to our genes, The significantly more common form of Alzheimer’s – LOAD – is not so clear in its origin. THE HYPOTHESIS Overtime it has come clear that three main lines of reasoning are emerging as to what is causing LOAD – and only one relates to genetics. 1) APOE-4 Gene Variant Theory: aka the “mutating gene hypothesis” 2) The Beta-Amyloid Cascade Theory: aka the”protein-gone-wrong hypothesis” 3) The Opportunistic Pathogen Theory: aka the “microbial/infectious hypothesis” – which is the theory The CAD Foundation and the University of Minnesota are working together to figure out. The first two theories hinge on the idea that the human body is the problem, that in the last 100 years – changes to our DNA are now manifesting in diseases such as Alzheimer’s. The last theory hinges on the idea that environmental factors (such as what we are eating, and our lifestyle choices) are the issue. And that in the last 100 years changes in society (many considered “modern conveniences” are now manifesting in diseases such as Alzheimer’s. DISCLAIMER Copyright © 2022 Curing Alzheimer’s Disease [EIN #88-3154550] All Rights Reserved. This information is not designed to replace a physician’s independent judgment about the appropriateness or risks of a procedure for a given patient. Always consult your doctor about your medical conditions. Curing Alzheimer’s Disease.com does not provide medical advice, diagnosis or treatment. Use of the site is conditional upon your acceptance of our terms of use.
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When we think about the immune system, most of us picture white blood cells fighting off a cold or healing a cut. But here’s something crucial to keep in mind: your brain has its own immune system that works entirely different than the rest of your body. As the CAD Foundation funds research into the microbial / infectious hypothesis of Alzheimer’s, this idea of the brain having its own immune system is very important. Especially in instances where something foreign ( environmental toxin or even a bacterial, viral, or fungal cell ) gets past the blood brain barrier where it’s not supposed to be. You’d be lost if your brain didn’t have its own immune system. Literally. Instead of white blood cells, your brain uses immune cells called microglia to monitor, protect, and support its neurons. Microglia are essential for keeping neurons healthy — and alive. When neurons become sick or die, it affects how we think, feel, and function. That’s why keeping them safe is so important. Let’s break the brain’s immune system down cell by cell. And then look at what happens when things go awry. What Are Glial Cells? Microglia are just one type of glial cell — they are a group of non-neuron cells that play critical support roles in the brain. While neurons do the thinking, glial cells keep everything running smoothly. They provide structure, deliver nutrients, clean up waste, and help defend the brain. Interestingly, glial cells outnumber neurons in many parts of the brain. The word “glia” means “glue” in Greek—but they do way more than just hold things together. There are several types of glia, but for brain cleaning and immune function, the most important are: These tiny (thus the term micro), spider-shaped cells are basically the brain’s built-in security guards. They’re constantly patrolling, looking for anything that shouldn’t be there ( dead cells, waste products, misfolded proteins, excess neurotransmitters and pathogens ). If they find any of these “problems” in the brain, they sound the alarm and start cleaning things up. But microglia aren’t just there for emergencies. They also help keep your brain working smoothly by pruning weak or unused connections between brain cells. Kind of like a gardener trimming branches to help the tree grow better. Astrocytes: The Helpers That Do Everything Astrocytes are larger than micogroglia and more star-shaped, with long, branching arms that spread out to support and connect many neurons at once. They act like the brain’s caretakers, overseeing and maintaining the environment where neurons live and work. Here are some of their chores: Learning & Healing: BDNF and Cytokines So we were just talking about cells a moment ago. But another important player in your brain’s immune system are molecules. Keep in mind: cells are anywhere from 1,000 to 100,000 times larger than molecules. But smaller size doesn’t mean less power. Let’s learn more about two very important molecules used by the brain’s immune system. BDNF (brain-derived neurotrophic factor) is a mouthful, but think of it as Miracle-Gro for your brain. It helps your brain grow, heal, and learn. You make more BDNF when you exercise, sleep well, or challenge yourself to learn something new. Interestingly, and to be discussed in greater detail – chewing your food well boosts BDNF levels! BDNF doesn’t just help your brain grow — it also helps keep inflammation in check. When BDNF levels are healthy, it protects neurons from stress and reduces the risk of overactive immune responses in the brain. Low BDNF has been linked to higher inflammation, brain fog, and mood issues. In a way, BDNF helps keep the brain’s immune system balanced — encouraging healing, not harm. Cytokines – which are also tiny molecules in your brain – can be thought of as “text messages” your immune system uses to send alerts. Some are anti-inflammatory—they help calm things down and keep your brain balanced. They work in harmoney with BDNF. Other types of cytokines are actually pro-inflammatory—they jump into action when there’s a threat, like you’d find with an infection. But when your body sends too many of the wrong (text) messages (especially during stress, poor sleep, or chronic infections), it creates ongoing inflammation in the brain. That kind of constant “brain fire” can damage brain cells and make it harder to think clearly or remember quickly or even remember at all. So, who sends out these cytokine alerts? Think of your brain like a high-tech city. When there’s trouble—like a virus sneaking in, a head injury, or a long-term bacterial infection (like see with gum disease)—your brain’s security guards (remember the microglia from earlier?) sound the alarm. Microglia are like firefighters and paramedics rolled into one. They scan the scene, then call for cytokines to come and check it out. Some cytokines – are just informational… Others hit the panic button and scream… …in effort to bring in heavy reinforcements. If it’s a quick fix—like clearing out a dying cell—the cytokine response wraps up fast. But if the problem is ongoing and unresolved, like with chronic bacterial infection, the alerts don’t stop. The emergency system keeps firing, and eventually, it goes haywire. Instead of helping, it starts harming healthy brain cells—causing swelling (inflammation), confusion, and over time, even memory loss. And then there’s the Night Crew: The Glymphatic Team who clean while you sleep Ever wonder why sleep is so important? Well, while you’re deep asleep, your brain uses it’s own type of cleaning system to collect and flush out waste, including that metabolic debris mentioned earlier as well as any other “junk” left behind by immune battles that took place during your day. It’s called the GLYMPHATIC SYSTEM. Think lymphatic (which in the body is how we remove impurities) just this system starts in your brain and is powered by glial cells. Eventually, the glymphatic system dumps the misfolded proteins, toxins, debris, and dead cells off to the body’s lymphatic system so it can finish removing all that garbage We will go into
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If you want to decrease your chances of contracting Alzheimer’s, then it’s critical that you eat a well-balanced, low-to-no-sugar, diet that pulls mainly from whole foods (meaning not processed like, say a frozen meal). Fruits and Vegies, which are high in fiber, should be a focal point of every meal, along with reasonable portions of lean meat and fish – or legumes and nuts for those choosing a more vegetarian or vegan lifestyle. Back in 2015 (so not too long ago!) a researcher in the fields of nutrition and epidemiology came up with a diet that brings all this together. Called the MIND diet, which is short for Mediterranean-DASH Intervention for Neurogenerative Delay diet, this approach to nutritious eating basically combined the best aspects of the Mediterranean diet with the Dietary Approaches to Stop Hypertension (DASH) diet. Intended to slow the cognitive decline that comes with aging, the MIND diet continues to rise to the top as the best diet for preventing and slowing Alzheimer’s Disease. The MIND diet is a unique version of the Mediterranean diet protects the brain and can help in preventing Alzheimer’s Disease. Next up: limit your sugar intake We aren’t talking complete elimination of all sugar, but being aware of your intake and reducing unnecessary sugar intake helps reduce inflammation and over all acidity – both of which are a benefits of our Alzheimer’s Prevention Strategy. Read product labels – you don’t need sugar in your ketchup. You don’t need sugar in your bread. Use healthier alternatives like honey when possible (which is a natural antibiotic). Over time, you’ll crave sweets less and eventually you will actually begin to prefer savory foods over goodies like cake and ice cream. Probiotics are a key ingredient in many Mediterranean Diets from around the world…here’s why: Another part of our Alzheimer’s Prevention Strategy is the deliberate incorporation of good bacteria into your diet. And If we could buy stock in this company, we would. This particular Probiotic, called Kefir, which is found in the yogurt section of most grocery stores, has the single best pro-biotic to fight Alzheimer’s Disease – Lactobacillus Planetarium. We discovered Kefir when we looked at the variety of Mediterranean Diets out there to see if any version stood out with better outcomes. After a lengthy review, we discovered that the regions that incorporate Kefir in their diet had the lowest Alzheimer’s incidence – hands down. Looking deeper into why this is the case, we discovered that L. Planetarium (the main bacteria contained in the Kefir product pictured here) eats up the food source for all the bad bacteria that causes IBS and can possibly cause Alzheimer’s – which is a natural way to defend yourself that protects both the gut and the brain. For those of us who cannot tolerate dairy, Gut Belly makes a dairy free pill option: https://shop.goodbelly.com/mango-juicedrink-32-oz Another great tip: Change your oil to Olive Another great Alzheimer’s Prevention Strategy that’s very easy to incorporate into your diet is substituting butter and margarine with Olive Oil when possible. In fact, across the board, all researchers agree that the Olive Oil found in the Medi-diet is a crucial ingredient to great brain health and placidity. As with everything, moderation is key. Eating fish twice weekly – limit red meat is also considered very brain-healthy And our final Alzheimer’s Prevention Strategy is to consider adding Fish and seafood to your diet. As with olive oil, wild-caught fish is high in Omega-3 fats, which has been proven to be very protective for our brains. Not so much with farm-raised fish (which is indicated on all packages now). Farm-raised fish is actually high in the wrong fat – Omega-6 – which is actually harmful to us. Eating fish at least twice a week as your protein is not only brain smart, but belly beneficial. Try Tuna in the can, or Salmon, Cod or Tilapia, Shrimp, Scallops – the good-for-you options are so vast and exciting!
Mind Your Fuel – Diet is a critical component to preventing Alzheimer’s Read Post »
Donepezil is one of the most widely prescribed drugs for the treatment of Alzheimer’s. Its basis in medicine started back in 1976 when two researchers discovered a marked reduction in the activity of enzymes involved in the metabolism of the neurotransmitter Acetylcholine in brains of deceased patients with Alzheimer’s Disease (AD). This finding led to the hypothesis that AD was caused by a “cholinergic system failure.” At the time, the best educated guess to remedy this theorized failure was to synthesize a new class of reversable Acetylcholinesterase inhibitors – one of which was Donepezil – that were trialed and eventually approved for widespread use for the treatment of AD. What we found a bit unnerving (no pun intended) is that nerve gas is also considered an Acetylcholine inhibitor. As are most insecticides. The main difference between acetylcholine inhibiting drugs like Donepezil and insecticides like “Raid” is whether the drug is “reversible” or “irreversible” – a condition that boils down to the chemical structure of the acetylcholine inhibitor. Here’s a table that says it all. Our point in bringing this up is to clarify that Donepezil IS NOT NERVE GAS but that it is not a benign drug. It is affecting the single most prevalent neurotransmitters in our body controlling muscle movement. Unfortunately, years after the 1976 discovery, Acetylcholine inhibitors like Donepezil ended up not being the home run researchers expected. In fact, from the literature, it appears these drugs are barely a base hit. Studies (and there have been lots of them) show that Donepezil provides nominal improvements to cognition and with lots of potentially troublesome side-effects in the Short Term. More importantly, there are warnings after warnings indicating that this type of drug should not be used Long Term. Which raises the question of: were the scientists back in 1976 wrong? What if the reduction in enzyme activity is not due to a lack of cholinergic cells? What if it’s due to something else – like the blocking of signals by a self-preservation process within the brain? The real fact is: we still don’t know what is causing the synaptic loss in Alzheimer’s brains. What we do know is that cholinesterase inhibitors are proving to not be the utopic solution we initially thought they were. Still, Donepezil has been proven to provide a very slight cognitive improvement at the start of treatment. Which begs the question of “why”? So back to the literature we went and were not surprised to find that this class of drugs has recently been found to exhibit anti-inflammatory properties! This completely supports our hypothesis and further supports my dad’s very compelling story And this makes sense as scientists have now come to the realization that AD is a disease of inflammation – so of course a drug that reduces inflammation – even just a little – will have a positive impact on the patient. Here are just a few places where we are seeing references to the anti-inflammatory properties of Donepezil: Study 1: “Our data suggested that the anti-inflammatory effects of donepezil may be a novel mechanism on treating EAE and provided further insights to understand the donepezil’s neuroprotective activities in MS.” Study 2: “suggesting that DZ [Donepezil] directly prevents systemic inflammation.” Study 3: “Recently, anti-inflammatory and neuroprotective effects of the drug have been reported. “Cholinergic anti-inflammation pathway” has major implications in these effects.” We have firsthand experience with Donepezil. My dad – Dr. Crandall – took it for quite a while, and saw no cognitive improvement at the initial 5 mg dose and just a little at the 10mg. When he finally stopped taking it, we did see a little cognitive drop, which was quickly remedied by a 5 mg increase to his prednisone. But what was most interesting is that when dad stopped the Donepezil, we saw an improvement to his gate. This made us stop and think: is it possible the Donepezil had caused his jerky gate? How about other tell-tale signs of dementia that care-givers keep looking for: motion disturbances, balance issues/frequent falls, incontinence, tiredness/fatigue? From what we are learning, all of these could be explained by changes to the parasympathetic system. And Doneprezil is altering a crucial neurotransmitter of the parasympathetic system. And since no one has conducted a study on how this drug affects people after long term use – how do we really know if these physiologic changes are really the disease’s progression or actually the drug designed to slow the progression of the disease? Another thought we had, which will never be answered is: what would have happened if dad hadn’t been on steroids when he started Donepezil? Would he have experienced a bigger “bump” in cognition like others have reported when initially starting this drug? ARICEPT®(donepezil hydrochloride) Tablets, for Oral Administration DESCRIPTION ARICEPT (donepezil hydrochloride) is a reversible inhibitor of the enzyme acetylcholinesterase, known chemically as (±)-2, 3-dihydro-5, 6-dimethoxy-2-[[1-(phenylmethyl)-4-piperidinyl]methyl]-1H-inden-1-one hydrochloride. Donepezil hydrochloride is commonly referred to in the pharmacological literature as E2020. It has an empirical formula of C24H29NO3HCl and a molecular weight of 415.96. Donepezil hydrochloride is a white crystalline powder and is freely soluble in chloroform, soluble in water and in glacial acetic acid, slightly soluble in ethanol and in acetonitrile, and practically insoluble in ethyl acetate and in n-hexane. Notice the molecular weight (416 g/mol). From our experience, it’s a bit big for all of the drug to bust through the BBB – see our earlier post on antibiotics and molecular weight to see why we even mention this… Which means this common Alzheimer’s medication, or most of it, may not be getting into the brain and instead is relegated to run freely in the patient’s body. And since it’s method of action works on neurotransmitters critical to our parasympathetic system, while we are using the drug to (hopefully) improve brain function, we will also be inadvertently affecting bodily functions of heart rate, digestion, sweating, tearing, breathing, and muscle movement. Wow. When dad didn’t respond much to the drug, his prescribing doc told us that sometimes it takes a while for
auto-immunity is where your body attacks itself Now that it looks like the Amyloid Hypothesis is likely incorrect, an increasing number of researchers are postulating that Alzheimer’s Disease may be an auto-immune disease where the brain’s own defenses are what’s killing the brain. In this recent scientific article titled “Alzheimer Disease Pathogenesis: The Role of Autoimmunity” researchers point to the growing number of studies that suggest that we are heading in the wrong direction in treating Amyloid Beta as the genesis of this disease and instead should be heading in the direction of viewing Alzheimer’s as an immuno-response against the brain itself. Moreover, auto-antibodies, the researchers contend, might be the new Alzheimer’s diagnostic tool we’ll be using in the near future. As this line of reasoning takes off, be assured that we will begin seeing more studies and articles linking diseases like Diabetes and Rheumatoid Arthritis to Alzheimer’s Disease. But we are not so sure that connection can be made…and here’s why: If having an auto-immune disease was key to whether you would develop Alzheimers, then it would reason that all auto-immune diseases would carry the same or very similar risks for developing Alzheimer’s Disease. Which is absolutely NOT the case. In fact, many auto-immune diseases don’t even show up as co-morbid conditions to Alzheimer’s – meaning many people dying of Alzheimer’s don’t have a single auto-immune disease and vise-versa…many people with an auto-immune condition never contract Alzheimer’s. Therefore, we feel this inconsistency begs us to look closer at those auto-immune diseases THAT DO show up as co-morbid diagnosed conditions for keys as to why a high number of individuals with these diseases go on to develop Alzheimer’s. And we contend that the overlap between the following auto-immune diseases and Alzheimer’s may be locked up in other risk factors that coincide with these auto-immune disorders…the top two being age and being female at birth. The Curing Alzheimer’s Disease Foundation is dedicated to helping explain the connection between Autoimmunity and Alzheimer’s. In this recent blog post, we delve into the fascinating theory that looks at a specific immune cell that, in some people is over produced – and could be contributing to this still unknown link. THE FOLLOWING AUTO-IMMUNE DISEASES ARE LINKED TO ALZHEIMER’S Periodontal Disease In as far as autoimmunity and Alzheimer’s goes, Periodontal Disease (PD) has the highest co-morbidity with Alzheimer’s Disease of all auto-immune disorders. We believe this is because: if you have PD, you have a type of bacteria that can also cause Alzheimer’s. We saw this in the dental clinic daily – in fact, we could frequently predict who would be suffering from dementia / or was already suffering from dementia just by looking at their periodontal-charting! Advanced age with deep pockets over a long period of time = Mild/Moderate Cognitive Impairment or even Alzheimer’s Disease. In fact, it was rare where this wasn’t the case. Taken further, if a tooth (or many teeth) were lost due to Gum Disease then it was a guarantee that if the the individual was older (60+) they were already starting to fail cognitively. Wow. We will bring you more information on this in a future blogpost. Diabetes Diabetes – in both forms (type I and type II) – is close to the top of the list of auto-immune diseases that are linked to Alzheimer’s. Which begs the question: why do so many people with Alzheimer’s also have Diabetes? We think the answer is simpler than the hard-thinking research world wants it to be: We believe the parallel is due to what happens to diabetics as this disease progresses. One of the most irritating symptoms of Diabetes is xerostomia – commonly known as Dry Mouth. Now, when you have no/low saliva, you will inevitably develop Periodontal Disease because the lack of saliva (saliva is what keeps the mouth PH basic), the PH of your mouth becomes acidic. And when the PH of your mouth becomes acidic, the bad (harmful) bacteria overgrow and the good (harmless) bacteria die. Tooth decay and Periodontal Disease (PD) ensue, the later of which (as we just covered) increases your risk of developing Alzheimer’s. Rheumatoid Arthritis (RA) Lupus Sjogren’s Syndrome For the longest time, researchers have been documenting a strong association between this form of autoimmunity and Alzheimer’s Disease. We agree that Sjogren’s Syndrome (SS) is risk actor – partly because it’s strikes women far more than it does men – see risk factor: biological sex. But mostly because of what it does to the body. Just as with Diabetes, SS, by nature, reduces saliva (among other autonomic functions) and in so doing, reduces the oral PH. This, we contend, is why this disease appears to be a strong risk factor Copyright © 2022 Curing Alzheimer’s Disease [EIN #88-3154550] All Rights Reserved. This information is not designed to replace a physician’s independent judgment about the appropriateness or risks of a procedure for a given patient. Always consult your doctor about your medical conditions. Curing Alzheimer’s Disease.com does not provide medical advice, diagnosis or treatment. Use of the site is conditional upon your acceptance of our terms of use.
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The odds are not favorable for women when it comes to contracting Alzheimer’s Disease. Women contract AD earlier in their lifespan, and unquestionably much more frequently (try two times more) than their male counterparts. Interestingly, not until the 8th decade (your eighties) does the rates of AD balance out between the different sexes, at which times your odds of getting AD at this point in your lifespan becomes identical for both men and women. Fact: Being biologically Female doubles your Alzheimer’s risk – and here’s possibly why: Study upon study finds that an increased risk of Alzheimer’s is linked to Menopause. Furthermore, the spike in cases for women seems to have been kickstarted by the 2000 Women’s Health Initiative (WHI) that recommended that women discontinue hormone replacement therapy (HRT) based on one rogue study that suggested hormone replacement caused cancer and heart disease in women. The HRT ban happened instantly and worldwide. And 10-15 years later, we begin to see a significant spike in Alzheimer’s diagnosis and deaths in our female population. That 2000 study has since been replicated over and over and over again – and not one of those follow-up studies has shown that HRT yields the same heightened risk for cancer and/or heart disease. Yet doctors worldwide continue to deny women the right to receive the estrogen and progesterone that their bodies are deficient in. Now, there still remains a very serious concern within the medical community regarding prescribing HRT to women with a history of cancer or heart disease. In fact, the women in the earliest study who developed cancer and heart disease had not been selected out of the study (which is why it is considered a flawed study). That valuable data though, raises concern for this subset of women who are at a greater risk due to their underlying conditions or genetic propensity. In those instances, it would be critical to consult with your medical doctor on alternatives to HRT that can boost your estrogen levels – such as gaining more of this hormone naturally from your food. Here’s an article regarding the eight foods high in estrogen that you may find interesting. (2) Good to know: Menapause is caused by the full depletion of eggs from a woman’s ovaries – as women are born with the total number of eggs they will cycle through, a woman’s predicted age of Menapause is controlled by 1) age of first period 2) age when her last egg is released 3) whether she has received any fertility treatment that would expedite entrance into menapause. (1) And of course, as genes play a role, looking to your mother’s path toward menopause will serve as a guide to the approximate age you will enter into menopause yourself. We will be publishing a blog post soon on Menapause and how this hormone deficiency syndrome impacts a woman’s risk for developing Alzheimer’s Disease. So check back or subscribe to our blogsite to catch it when it comes out. (1) Postmenopausal syndrome https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539866/ (2) Top Foods High in Estrogen https://www.webmd.com/diet/foods-high-in-estrogen
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Based on our knowledge and experience, here’s what we think you would want to know about Late Onset Alzheimer’s Disease (LOAD). In a follow up article (Part II), we will offer advice gained from experience and current literature that can help you possibly slow the disease down until a Cure is available for widespread use. But for now, we’d like you to – 1) Know that there are two forms of Alzheimer’s – Early Onset Alzheimer’s Disease and Late Onset Alzheimer’s Disease. Early Onset (which is rare) occurs before age 65. Late Onset Alzheimer’s (which is what most of us think of when talking about Alzheimer’s) occurs after age 65. (1) This article focuses on this second form of Alzheimer’s Disease. 2) Know that without an autopsy, a clear-cut diagnosis for this disease is impossible. Therefore, it’s critical that other medical reasons that can look like early-stage Alzheimer’s disease have been ruled out. Conditions with similar cognitive symptoms include: depression, stress, diabetes, thyroid disfunction, liver or kidney disease, vitamin deficiencies, even exposure to low levels of carbon monoxide. These are easy tests to perform and will give you the reassurance that a presumed Alzheimer’s diagnosis is truly accurate. 3) Know that Primary Care/Family Practice/Internists are in no position to diagnose AD– and after ruling out all medical and psychological explanations for your decline – their duty is to refer you to a Neurologist for further testing and treatment. 4) Know that many people over the age of 60 have some Alzheimer’s pathology already in their brains (2a) and yet they show no signs of cognitive impairment. So, you have more and are seeing a decline in your ability to think – it’s time to do something about it. 5) Know that Alzheimer’s Disease is generally contracted 10-15 years before symptoms force a diagnosis. The median age for diagnosis is 79.9 (2), therefore the median age for contracting this disease is estimated to be 65-70 years of age. 6) Know that one of the top risk factors for Alzheimer’s is having gum disease. (3) (4) A fact long suspected in Dentistry, and just now entering the science community. 7) Know that Alzheimer’s Disease skyrockets 10-15 years after a country changes their position on prophylactic antibiotics during dental procedures. It’s too consistent to be coincidental. 8) Know that Alzheimer’s Disease began to skyrocket 10-15 years after our medical community stopped endorsing Hormone Replacement Therapy for post-menopausal women. 9) Know that most auto-immune diseases that are considered risk factors for Alzheimer’s are risk factors because they overlap with the higher risk that gender plays in contracting Alzheimer’s. Being female increases your risk of contracting Alzheimer’s substantially. And women make up the bulk of those diagnosed with Sjogren’s Syndrome, Rheumatoid Arthritis, Lupus, even type II diabetes that strikes after menapause. 10) Know that aging is your number one risk for contracting late-onset Alzheimer’s Disease. This is LARGELY because of something called Senescence – which is defined as the loss of our cell’s ability to divide and grow. This, in turn affects every biological system in your body – in the instance of Alzheimer’s Disease, senescence impedes your brain’s ability to protect itself from foreign pathogens like bacteria. 11) Know that Alzheimer’s is a disease of inflammation. Which is why the most commonly prescribed Alzheimer’s drugs (that have been shown to reduce brain inflammation), seem to work initially (5). But as the diseased brain becomes more inflamed, the effectiveness of these drugs quickly becomes insufficient. Which is why you should …. 12) …Know that research continues to prove that current Alzheimer’s drugs have little to no positive effect (6). Yet these drugs come with a very serious list of side effects. Therefore, you should be challenging your provider to show you the studies that support his/her recommendation that you should be taking these drugs. You will find that no Alzheimer’s drug has been studied longer than 5 years. So, no one really knows what they are doing to your brain’s chemistry long-term. 13) Know that the idea that Alzheimer’s is inherited can be disproven by statistic– 70% of Late Onset Alzheimer’s Disease (LOAD) cases have no family history for Alzheimer’s (7). So, it’s time to stop blaming genetics and time to start looking for what you can do now. Stay tuned for our second article in this series that will help offer ideas on what you can do now to potentially protect yourself against Alzheimer’s Disease. Feel free to visit our website at www.CuringAlzheimersDisease.comfor more information, and be sure to subscribe to this blog www.Curing-Alzheimer’s.com for updates on what is published next. # # # Citations: (1) Types of Alzheimer’s Disease (2a) Non-Demented Individuals with Alzheimer’s Disease Neuropathology: Resistance to Cognitive Decline May Reveal New Treatment Strategies (2016) (2) Time from diagnosis to institutionalization and death in people with dementia (2020) (3) ) Oral bacteria may be responsible for Alzheimer’s disease – Harvard University 2019 (4) Large study links gum disease with dementia – NIH 2020 https://www.nia.nih.gov/news/large-study-links-gum-disease-dementia#:~:text=Among%20those%2065%20years%20or,to%20further%20increase%20those%20risks (5) Donepezil doesn’t cure Alzheimers, it just treats AD inflammation 2020 (6) Current Alzheimer’s drugs do little to help patients – 2020 (7) Maternal transmission of Alzheimer’s disease: Prodromal metabolic phenotype and the search for genes About the author: Anna Shelander is a journalist and question-asker who rarely accepts “no” for an answer. Which is why, when her dad (Dr. Crandall ) became ill with an unexplainable disease, he asked her to come along for the ride. The two worked unsuccessfully within the medical community to find a diagnosis, then branched into the research community where answers finally began to appear. It was at this level of science that Anna and her father began to parse together the drug protocols that dramatically improved his cognition. Disclaimer No content on this site, regardless of date, should ever be used as an absolute substitute for direct medical advice from your doctor or other qualified clinician. This article should be viewed as advice that is based on current research regarding the potential to slow and possibly prevent Alzheimer’s Disease. Copyright © 2022 Curing Alzheimer’s Disease [EIN #88-3154550] All Rights Reserved. This information is not designed to replace a physician’s independent judgment about the appropriateness
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