Infection Possible Cause of Alzheimers 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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Yoga Lowers Heart Disease Risk as much as Conventional Exercise

by Nina

Walk Along the Banks of the Seine Near Asnieres by Van Gogh

“A recent review of yoga and cardiovascular disease published in the European Journal of Preventive Cardiology indicates that yoga may help lower heart disease risk as much as conventional exercise, such as brisk walking.” — Julie Corliss, Harvard Health Blog

Well, that sentence from More than a stretch: Yoga’s benefits may extend to the heart certainly merits a closer look, don’t you think? Because even though we’ve written extensively about the benefits of yoga for cardiovascular health (see About Yoga for Heart Health), I’ve never actually seen scientific proof that yoga really is as good for heart health as—as this quote says—a brisk walk.

The report on the Harvard Health blog was referring to the study The effectiveness of yoga in modifying risk factors for cardiovascular disease and metabolic syndrome: A systematic review and meta-analysis of randomized controlled trials in the European Journal of Preventive Cardiology. This turns out to be one of those review studies that assesses other existing studies, in this case, 37 randomized controlled trials (RCTs) in the systematic review and 32 in the meta-analysis, which can provide a very good picture of what the current research is turning up. The review study itself says:

“Whereas previous reviews have looked at a single or a few risk factors, our review updates the existing literature and encompasses numerous CVD and metabolic risk factors that can be used to calculate overall CVD risk.”

The studies that were reviewed looked at different types of yoga, including both gentler and more energetic styles, and the participants ranged from young, healthy individuals to older people with health conditions. Interestingly, there were no restrictions on the frequency of yoga practice or its duration. (Although I guess we can assume no studies were done with people practicing yoga just once a month!) In the review, the control groups used in the studies were divided into aerobic exercise (physical training, aerobic exercise, cycling, running, brisk walking) and non-aerobic exercise groups. This allowed the researchers to estimate the effectiveness of yoga practice compared to both active controls and versus non-active controls.

Overall, the people who did yoga improved in several factors that affect heart disease risk: losing an average of five pounds, lowering blood pressure by five points , and lowering their levels of harmful LDL cholesterol by twelve points. And no significant difference was found between yoga and exercise!

For those of you who are interested in more detail, the study itself concluded that compared to non-exercise controls, yoga showed significant improvement for:

• Body mass index (−0.77 kg/m2 (95% confidence interval −1.09 to −0.44))
• Systolic blood pressure (−5.21 mmHg (−8.01 to −2.42))
• Low-density lipoprotein cholesterol (−12.14 mg/dl (−21.80 to −2.48)) and high-density lipoprotein cholesterol (3.20 mg/dl (1.86 to 4.54))
• Body weight (−2.32 kg (−4.33 to −0.37))
• Diastolic blood pressure (−4.98 mmHg (−7.17 to −2.80)), 
• Total cholesterol (−18.48 mg/dl (−29.16 to −7.80)), 
• Triglycerides (−25.89 mg/dl (−36.19 to −15.60)
• Heart rate (−5.27 beats/min (−9.55 to −1.00))

The original review study concluded: 

“Our review finds emerging evidence to support a role for yoga in improving common modifiable risk factors of CVD and metabolic syndrome.

“We believe that these findings have important implications for the acceptance of yoga as an effective therapeutic intervention. This review demonstrates the potential of yoga to have an impact on concrete, physiological outcomes that represent some of the greatest health burdens today.”

The Harvard Health blog interviewed Dr. Gloria Yeh, a co-author of the review and an associate professor of medicine at Harvard Medical School. She said, “Yoga is unique because it incorporates physical activity, breathing, and meditation.” And she explained that each of these elements positively affects cardiovascular risk factors, so combining them was bound to show a benefit. 

See About Yoga for Heart Health for an overview of and links to all the posts—including practices designed especially for heart health—that we have on our blog.

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