Alzheimer’s Disease, AD, is one of the fastest growing diseases of the aging population. It is estimated that 5 million people are diagnosed with Alzheimer’s Disease, with at least 60% of those being women. It is estimated by 2050 about 15 million will be diagnosed. With so many patients presenting with dementia and Alzheimer’s Disease we must, by now, have a solid grasp on the cause and be working on a treatment…right? Wrong.
We have yet to discover a specific pathogen or genetic factor that causes Alzheimer’s disease. There are risk factor genes such as APOE (type 4) and the accumulation of amyloid beta protein, and neurofibilary tangles in the brain, but then there are also patients that have these factors and never develop Alzheimer’s or even cognitive decline. There must be something else. We do know the overall mechanism of how this disease manifests itself. Believe it or not it’s the exact same process that happens in all diseases! Inflammation is the name of the game and in respect to Alzheimer’s we are talking about inflammation in the brain. Anything that can trigger the inflammatory cascade has the propensity to develop into Alzheimer’s regardless of its relationship. For example, diabetes is thought to be more of a “body disease” rather than a brain issue; yet patients with diabetes raise their risk for Alzheimer’s by 200%! In fact, you do not even need to have the diagnosis of diabetes to double your risk; nearly any form of dysglycemia (high blood sugar) will. Patients with fasting blood glucose levels over 90 mg/dL! That’s 36 points lower than the current reference range. For every point above 85 mg/dL you are putting yourself at substantial risk for chronic disease, which may include Alzheimer’s.
Like most conditions you need the “perfect storm” of variables, which include genetics, environmental triggers (commonly infections), and lifestyle to see full progression of disease. For some time it was thought that the APOE type 4 led to AD. Unfortunately, we do not see that direct correlation in the population. Someone who has 1 copy is at a 20-40% greater risk and patients with 2 copies can bring their risk up to 70%; but it does not mean because you have this gene you will undoubtedly develop AD. In fact, about 50% of patients who have APOE type 4 never develop AD.
Interestingly, patients who have APOE type 4 tend to experience more herpes viral infections, such as HSV-1 or cold sores. Herpes family viruses encompass some of the most common viral infections we know of. Epstein Bar Virus, EBV, is suspected to infect over 95% of the population. It is a latent, opportunist virus—meaning it can stay silent for years, even decades before it produces symptoms.
One study followed 512 elderly patients for 14 years. All began the study “dementia free.” At follow up, 77 had diagnosed AD. Blood was drawn and immune response to herpes simplex virus raised risk for AD by 2.5 fold independent of gender and genetics.
One of the hallmark signs of Alzheimer’s disease is plaque in the brain. These plaques are made of protein called beta amyloid. The complete story on why certain people trigger the production of excessive beta amyloid is still unknown but biopsy of plaques from AD brain revealed DNA from the herpes simplex virus in mouse brain models; suggesting that HSV may play a role in plaque formation or utilize the protein structure to replicate.
In fact there are many viral infections that we know of that affect the central nervous system: rabies, polio, west nile, and VSV, so it would not be far off to see some of these involved in the mechanism of Alzheimer’s Disease.
Viruses leading to autoimmunity and brain inflammation.
Viruses have many ways of infecting the brain:
- Direct infection – some viruses can cross into the brain freely
- “Trojan Horse” – the virus will hijack another cell which normally crosses the brain and hitch-a-ride
- Breakdown the Blood Brain Barrier – the protective barrier between the brain and the rest of body can be broken down by certain viruses
- Activation of immune system which triggers autoimmune antibodies
Some other genetic factors that could increase your risk for viral infections are defects in: Nitric oxide synthase, arginase, MTHFR, glutamate decarboxylase, and HLA. Defects in nitric oxide synthase, MTHFR 1298, and arginase could potentially raise serum arginine (which would lower lysine), leading to increase susceptibility to the herpes family of viruses as well as some other health complications.
Lyme disease is not classified as a virus; it is a bacterial infection of the species Borrelia burdorferi. Borrelia burdorferi has been found in post mortem plaques of Alzheimer’s brains. Borrelia has long been known to cross into the brain much like treponema pallidum, syphilis. Both infections cause direct infection of the brain as well as inflammatory response which can lead to memory lapse, depression, and anxiety.
Chlamydophila pneumonia, a bacteria that causes pneumonia was found to use microglia, neurons and astrocytes (all brain cells) as hosts for replication. This is speculated to trigger inflammatory markers and oxidative stress on neural tissue leading to beta amyloid plaques. They were able to culture the bacterium from the brain samples meaning that the infection was alive and active.
Even though these viruses and bacteria have not been found to be the causative agent in AD, they do activate the brains immune cells, the microglia, and cause brain inflammation.
So who is at risk? The data is pretty clear, anyone is at risk for dementia. Family history of the disease may indicate a genetic defect that has been passed through the generations; but once again it’s the environmental triggers that are necessary for the genetic expression. The patients that make me the most nervous are females—post menopausal with diabetes/ hyperglycemia and a history of cold sores. The current statistics of those who are diagnosed with AD fit this pattern.
If you are curious about your risk for Alzheimer’s disease, then some of the above should be ruled out and/or addressed to bring your risk score down. It is important to not get tunnel vision on the treatment for AD as this leads to neglect of other, seemingly unrelated, issues to go unattended. AD, like most, is a dysregulation of the immune system and the production of inflammatory proteins that trigger different pathogenic processes in the body. It is a complicated process that leads to Alzheimer’s, but that doesn’t mean it is a hopeless fight when the energy is directed towards the cause rather than the end manifestation of symptoms. Prevention, as always, is the best medicine. It is never too early to begin preventing these diseases of aging. The “watch and wait” model of medicine is antiquated and practicing in such a way should leave the Doctor watching and waiting for all his/her patients to return.
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Dr. Brett Wisniewski was born and raised in New Jersey. He attended Monmouth University where he received a Bachelors of Science degree in Biology with concentrated studies in chemistry. He has always gravitated towards the study of the human body and natural health. Dr. Wisniewski moved his family to Florida to further his studies at Palmer College Chiropractic where he graduated Cum Laude, with a Doctor of Chiropractic Degree. He then went on to study at the University of Florida where he completed his master’s degree in molecular cell biology with a concentration in immunology. Dr. Brett also holds diplomates from the American Board of Chiropractic Internists (DABCI) and the American Board of Clinical Nutrition (DACBN). Dr. Brett is both an instructor and administrator for multiple DABCI programs across the country and holds a seat on the executive board for the American Board of Clinical Nutrition.