Alzheimer’s Disease (AD) is a neurodegenerative disease that induces cell death and subsequent declines in processing and cognitive function. Alzheimer’s, a form of dementia, is widespread amongst aging populations. Nearly one out of every three elderly deaths are the result of Alzheimer’s Disease, making AD the 6th leading cause of death in the United States. Figures estimate that over 5 million Americans currently live with Alzheimer’s Disease, with this number projected to increase. Though the effects of Alzheimer’s are well documented, the exact cause of the disease is unknown. Recent findings, however, suggest that Alzheimer’s may be the result of microbial infections in the brain.
How is Alzheimer’s Formed?
Brain cells, known as neurons, relay information through specialized sites known as synapses. Synapses allow chemical structures, called neurotransmitters, to diffuse across neurons and relay communicative signals.
Traditional theories suggest that Alzheimer’s disease may be the result of blockage across chemical synapses. As individuals age, fragments of beta-amyloid proteins begin to clump together. These clumps combine to form chemically “sticky” plaques in the synapses between neurons. These plaques inhibit transmission and communication amongst neurons, leading to cognitive decline and cell death.
The “Pathogen Hypothesis”:
Recently, a group of clinicians examined the origins of AD. Their research, published in the Journal of Alzheimer’s Disease, suggests that Alzheimer’s may be the result of microbial infections in the brain. If true, these findings may hold substantial implications regarding the treatment of Alzheimer’s.
The “pathogen hypothesis” argues that Alzheimer’s is the result of microbial infection. According to research, individuals who possess a variant of the APOE gene are susceptible to neural infections from certain viruses or bacteria. There are three different alleles, or versions, of the APOE gene: APOE e2, APOE e3 and APOE e4. According to research, Individuals who possess the APOE e4 gene are at risk for virally induced Alzheimer’s.
One of the damaging pathogens identified by researchers is the HSV-1, or herpes simplex virus. The HSV-1 virus is already known to be responsible for cold sores and pneumonia. Individuals who possess the APOE e4 gene and who are infected with HSV-1 virus are especially at risk for AD. This phenomenon is described in detail in the Journal of Alzheimer’s Disease. “The microbial presence (HSV-1) in blood [plays] a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease,” says Resia Pretorius, a professor at the University of Pretoria in South Africa, “There is ample evidence that this (HSV-1 Virus) can cause neuroinflammation and beta-amyloid plaque formation.”
Correlation between the HSV-1 virus and AD are exhibited in other research as well. A 2015 meta-analysis found that viral infections, like those caused by the HSV-1 virus, are correlated to a 10-fold increase in Alzheimer’s occurrence (Maheshwari & Eslick, 2015). Along similar lines, a 1997 study found that participants who were infected with HSV-1 and possessed the APOE ε4 gene variation were twelve times more likely to develop Alzheimer’s Disease (Itzhaki, 1997). These findings are substantial, given the prevalence of the HSV-1 virus. Epidemiology reports show that nearly 65% of Americans have contracted the HSV-1 virus at some point in their lives (Wald & Coreys D, 2007).
Initial studies support the notion that the herpes (HSV-1) virus may prompt neuroinflammation and the buildup of beta-amyloid plaques in the brain. Such investigations suggest that microbial infections may be responsible for Alzheimer’s Disease and related dementias. Though emerging research is inconclusive, the pathogen hypothesis provides important direction for future analysis.