Infection: Possible Cause of Alzheimer's Disease?

by Ram

Roads and Fences by Marie Lossky

Alzheimer’s disease was first described in 1906 by a German physician Alois Alzheimer and the disease that got its name from this physician continues to baffle neuroscientists to date about the exact cause, cure, or treatment. Alzheimer’s disease (AD) is a progressive brain disorder that damages specific cells in the region of the brain called hippocampus. Death of neurons in the hippocampal area of the brain triggers short-term memory failure, and often the person's ability to do familiar tasks begins to decline as well. Alzheimer's disease also attacks other areas of the brain responsible for functions such as language and reasoning, resulting in the loss of language skills and judgment. As the disease progresses, patients often exhibit personality changes, emotional outbursts, and disturbing behavior, such as wandering and agitation. People with AD eventually require comprehensive care, thus the disease presents a considerable problem in patient management as well. It may sound strange that despite a century having elapsed since the disease was first described, there is still no cure or proper treatment for this disease.
According to recent statistical data, an estimated 5.4 million Americans of all ages have Alzheimer's disease. By 2050, the number of people with Alzheimer's disease may nearly triple, to a projected 13.8 million. In the last 10 years of the 244 compounds that went to clinical trials only one was approved. And that one approved drug works with limited efficacy only when given to patients during the early stage of the disease. Finding drugs for AD is especially difficult because: 

1. The exact cause of AD is not yet known.
2. The brain is relatively inaccessible, and harder to test and deliver compounds to.
3. No proper animal models exist that recapitulate? exactly the disease in humans.
4. Less is known about the biology of the condition.

 While the exact cause of the disease is still unclear, most of the attention has been driven towards a protein called beta amyloid, which forms toxic aggregates or plaques in the brain of AD patients. When not properly cleared, the toxic beta amyloid blocked transport of essential nutrients and disrupted communication between neurons that ultimately resulted in death of nerve cells, cognitive decline, and memory loss. Evidence suggests that amyloid is deposited early during the course of the disease, even before clinical symptoms appear. Thus, this protein became a major drug target in the search for a cure to Alzheimer’s, with pharmaceutical companies spending billions of dollars designing drugs that bind to and trigger clearance of the toxic beta amyloid. In all these trials, not only were these drugs ineffective in reversing the AD symptoms, in several cases, patients exhibited severe side effects very early on and the trials had to be abandoned prematurely. So targeting beta amyloid in patients with AD may not be the correct approach to stop the disease, and several researchers continued to debate passionately about the amyloid hypothesis while looking into other theories. 
Now a team of researchers is proposing a very different story. In a study published last week, the collaborative team from Harvard and MIT report that beta amyloid may actually have a critical neuroprotective role in the brain: protecting the brain from infections (bacterial or viral). The neuroscientists suggest that beta amyloid acts as a foot soldier by trapping potentially invading harmful bugs and alerting the other defense teams in the brain to their presence. By forming a mesh like structure, beta amyloid traps the microbes and prevents them from traveling deeper into the brain. The researchers also pointed out that animals that overproduced beta amyloid were more resistant to infections and had longer survival rates compared to animals that did not produce the protein. The higher the expression of beta amyloid, the greater was the protective effect from the infection, suggesting that beta amyloid acted as a natural antibiotic. This meant that getting rid of amyloid, as most drug trials tried in the past, could actually be dangerous, especially when the patient contracted any infection. 
So if beta amyloid is actually a protective protein, what eventually triggers Alzheimer’s disease? According to the researchers, the disease could be inadvertently triggered by an infection that causes the formation of excessive beta amyloid. As people get older and their immune system becomes increasingly compromised, it paves the way for microbes to sneak into the brain, resulting in an overabundance of the beta amyloid protein that exceeds the normal protective threshold. An excessive buildup of the protein may trigger the body’s own defense system to go awry that which we know as inflammation (see Chronic Inflammation and Yoga: Combating the Fiery Killer). Thus, what may be a neuroprotector, over time changes its face into a neurotoxic molecule. It is like the soldiers who stage a coup instead of defending their country. 
So what does this mean for pharmaceutical companies? Well, instead of attempting to completely eliminate the beta amyloid protein from the brain, drugs need to be engineered such that they dampen the beta amyloid levels to a stage where they continue to elicit the protective anti-infective properties. And what does it mean for people who have early stages of the disease? Or what does it mean for people who do not have the disease yet but who have a family history of AD? For now, some of us maybe able to avoid the chronic mind-ravaging effects of AD by making healthy changes to our lifestyle, remaining active, achieving ideal weight, reducing stress, and in some cases, taking vitamins, herbs and/or nutraceuticals that are recommended by a physician or licensed practitioner. The brain, like muscles in the body, requires exercise to remain functionally strong and resist infections. Stimulation of the brain increases the branching of brain cells that provide resilience to the brain and also support cognitive function. Thus, it is important to pursue intellectually challenging activity throughout life (see The Power of Mental Exercise, Part 1). 
Maintaining mental agility and learning new tasks as we age will also contribute to our own well-being and independence (see What is Healthy Aging, Anyway) Additionally, brain changes associated with meditation and stress reduction play an important role in slowing the progression of age-related cognitive disorders including AD. Furthermore, maintaining good sleep and sleep habits helps to clear out harmful toxins, a process that may reduce the risk of AD (see Sleep, Alzheimer's Disease and Yoga). If you’re having trouble sleeping, yoga’s stress management techniques can help quiet your nervous system so you fall asleep more quickly and more soundly (see Five Tips for Better Sleep). And if you'd like to add any additional practices to encourage brain health, start meditating on a regular basis (see Memory Loss—Meditation to the Rescue) and keep practicing your yoga asanas (see More on Yoga and Brain Strength: Neuroprotection). It’s not too late to start all these techniques and practices to keep a healthy brain and a strong mind, so better start today! 
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