What Is Alzheimer’s Disease?
Alzheimer’s disease (AD) is a crippling, chronic, and progressive neurodegenerative disease that is conventionally understood to be irreversible. It is characterized by memory loss, dementia, cognitive impairment, and the presence of amyloid plaques in the brain (1, 2). Approximately 5.1 million people over the age of 65 in the United States are diagnosed with AD, along with another 200,000 under age 65. This estimate is predicted to increase by 10 million in the next 35 years (3).
In addition to those diagnosed, this disease changes the lives of more than 15 million family members and caregivers. Today, the estimated annual out-of-pocket expense plus the value of the approximately 18.1 billion volunteer caregiver hours approaches a staggering $440 billion (4). Unless there are advances in the cause and treatment of AD by the year 2050, that number will approach $1 trillion. The Centers for Disease Control & Prevention reports that AD is the sixth leading cause of death in the United States (4, 5). James et al. (2014) suggest that AD-related deaths are underreported and estimate that it is actually the third leading cause of death after heart disease and cancer (6).
The History of Alzheimer’s Research
Alzheimer’s disease was first characterized and diagnosed over 100 years ago (7). Since that time, ideas on the pathology and treatment of AD have shifted from a focus on amyloid plaques in the brain as the cause (8), to misfolded tau proteins (9), to focus on the genetic heritability of the disease, to epigenetic influences (10, 11), to inflammation as a primary culprit (2), to medication-induced mitochondrial dysfunction (12), and to metabolically influenced mechanisms (13, 14, 15).
The breadth of Alzheimer’s research speaks to how elusive this disease really is. Despite the uncertainty of specific causal mechanisms, there are currently five prescription drugs that are used to combat the symptoms of AD. The last drug approved to treat the symptoms of Alzheimer’s disease was brought on the market in 2003.
The overall success rate over that period of time was measured to be 0.4 percent (99.6 percent failure) (1).
Recently, a group of 33 Alzheimer’s researchers joined forces to raise awareness about a neglected piece of the Alzheimer’s puzzle: the correlation between the manifestation of this disease and the microbial world (16).
What If Alzheimer’s Is an Infectious Disease?
An infectious disease is one that is caused by a pathogenic microbe and may be spread directly or indirectly (17). Infectious disease rates have plummeted over the course of the past century due to advances in sanitation, vaccination, and treatment (18). Historically, once a disease is identified to be infectious in origin, treatment and prevention protocols have been successful.
The idea that Alzheimer’s disease may be an infectious disease is supported by a number of observations. There have been many correlations between common infectious and immune-challenging agents and the diagnosis of AD (16).
Could Alzheimer’s be an infectious disease? Some research says yes.
“Seeding” Alzheimer’s disease in mice. Researchers have successfully created senile plaques associated with AD by infusing dilute fluid from the neocortex of Alzheimer’s patients into mice (19). These results highlight a key pathogenesis for neurodegenerative disease in mice and open up avenues for research in human subjects.
Type 2 diabetes and Alzheimer’s disease. A link between type 2 diabetes and AD has been suggested as both diseases present with local inflammation and amyloidosis (misfolded proteins) and are both associated with the presence of a common microbial community that includes Chlamydophyla pneumoniae, Helicobacter pylori, and spirochetes (20).
Periodontitis and Alzheimer’s disease. There is a correlation between the diagnosis of AD and periodontitis (21). Researchers hypothesize that the microbes living in dental plaque biofilm invade the brain via the bloodstream or peripheral nerves and promote inflammation of the central nervous system, which is known to be associated with cognitive decline (21, 22, 23).
Herpes simplex virus 1 and Alzheimer’s disease. Herpes simplex virus type 1 (HSV1) is quite common in the general population; roughly 70 percent of people over the age of 50 have been exposed to it. HSV1 was first proposed to be associated with AD nearly 35 years ago (24). This hypothesis was made plausible when researchers discovered a technique to test for the HSV1 virus in the human brain (25). After adjusting for known risk factors (age, education, APOE status) Letenneur et al. (2008) discovered a significant correlation between patients with primary or reactivated HSV1 (as measured by immunoglobulin M) and AD diagnosis (26, 27).
Atherosclerosis and Alzheimer’s disease. Atherosclerosis has been compared to AD because both diseases present with inflammation; are associated with viral and bacterial infection, including HSV1 and Chlamydophila; and are characterized by plaque formation. Researchers hypothesize that both are caused by a chronic immune challenge (infection) that induces cholesterol 25-hydroxylase expression (plaque) to protect the body locally against infectious agents (28).
Biotoxins and Alzheimer’s disease. A connection has been made between biotoxin exposure and a distinctive type of AD that affects younger people that is characterized by some combination of stroke-like speech impairment, partial Gerstmann’s syndrome, impaired ability to read, inability to interpret visual information, or impaired motor skills. This AD-type is “cortical” (14) and has now been reported in the literature as “inhalational Alzheimer’s disease” (IAD), a manifestation of chronic inflammatory response syndrome (CIRS) resulting from biotoxin exposure (29, 30).
If AD Is Infectious, What Can You Do?
It is not inaccurate to say that “health” is the best way to fight infection, but more specifically, a thriving, functioning immune system and a mindful perspective (31). An immune system under constant stress will slowly and steadily begin to malfunction over time, making our bodies more permissible to strange and pathogenic ecosystems (32, 33).
The best way to support your immune system and overall health is to provide your body with the information that it needs to operate and to make sure that the information delivered is in fact received. The receipt of this information is influenced by your overall gut health (34). Once gut health is considered, the required information from your environment comes from:
- Nutrient-dense, whole foods. Hyper-concentrated food products (sugar, flour, processed seed oils) containing preservatives and artificial ingredients crowd out nutrients that only come from whole foods.
- Quality sleep. Reconnecting with your natural circadian rhythms to facilitate growth, repair, and cellular cleanup in your body is incredibly important immune support. (35)
- Natural and functional movement. Frequent, low-intensity natural movement distributed throughout the day supports a dense vascular network that assists in the delivery of nutrients to your cells and the removal of waste from them. (36)
- The sun and spending time in natural environments. Vitamin D synthesis from exposure to the sun is an important part of overall health. Spending time in natural environments is not only nutritious but can expose you to immune-supportive microbial communities and relieve you of chronic stressors that are present in indoor environments. (37)
- Support from your community. There is a large body of evidence illustrating the importance of feeling socially connected for your overall health. Lack of connectedness and support decreases your immune function. (38)
- Happiness and a sense of purpose. Immune stressors come in all forms, and emotional stressors play a large role. Your mindset influences the amount of perceived stress you have, which can have a profound influence on your immune health. (39, 40).
Although I believe that Alzheimer’s (as well as most other modern diseases) is multifactorial and has several causes, the recognition that Alzheimer’s disease may be the result of a progressive, chronic infection may initiate new treatment options for this debilitating neurodegenerative disease.