German doctor Alois Alzheimer discovered the disease in 1906, when he examined a post-mortem patient who had died with an unknown mental illness. Dr. Alzheimer found unusual clumps of protein plaques in the patient’s brain. These plaques are made up of clustered proteins and are today noted as a clear sign of the disease with new brain scan (PET) and imaging (MRI) techniques being developed to help with early detection of the disease. Unfortunately scientists have long been debating whether these protein plaques cause the disease or are simply a by-product of it. As this debate continues, the elderly continue to develop Alzheimer’s disease (AD) at an alarming rate, while the speed at which research studies provide an answer feels like it is crawling in comparison.
So what could be causing these plaques, and therefore causing Alzheimer’s? Normal brain function and structure are disrupted as a result of inflammation and one example is that inflammation causes proteins in the brain called amyloid beta proteins to mis-fold, meaning their configuration is not normal. Mis-folded amyloid beta proteins have a critical role in the development of Alzheimer’s. Their abnormal configuration causes them to cluster together, forming plaques, which kill important nerve cells in the brain. Inflammation is now understood to be a major factor in the disease process and possibly a cause in the damage that occurs in the brain and leads to Alzheimer’s.
A recent study showed that some markers of inflammation were present in patients with either Alzheimer’s, vascular dementia or mild cognitive impairment.(1) Since these three neurological disorders share similar features related to diminished brain function, it was not a surprise that all three could be linked to inflammatory processes. Research into the role of inflammation in AD is further evidenced by studies using common over the counter anti-inflammatories (NSAIDs)*. The Baltimore Longitudinal Study of Aging actually showed that the risk for developing AD is reduced with the use of NSAIDs, and the reduced risk was directly proportional to duration of use of the NSAIDs.(2) The authors of the study concluded that the stage of the disease process leading to AD is characterized by an inflammatory process. Many more studies have since established the link between inflammation and AD. The November 8, 2001 issue of the journal Nature, suggesed that NSAID therapy has a direct impact on the cause of the disease. However, other research indicates that other mechanisms independent of the anti-inflammatory effects of NSAIDs are taking place. (3) While more research is needed to clarify how NSAIDs are a benefit in the prevention of AD, the consensus is that inflammation is a central process in the development of AD.
Are NSAIDs a viable solution to prevention of AD? Prolonged use of NSAIDs is not advisable or recommended. Long term NSAID use can lead to damage to the digestive tract. More serious side effects of NSAID use include heart failure, liver disease and kidney damage. It is just as important to note that NSAIDs have failed to alter the disease process once it is established, in at least two trials. There are many natural inhibitors of inflammation that are safe and as effective than NSAIDs that I will be sharing about in future posts. Even more important is working with a practitioner that will evaluate any chronic inflammatory processes that you may not be aware of.
* NSAIDs are known to inhibit enzymes called cyclooxygenases (COX), which are integral in inflammatory responses.
1. Oztürk C, Ozge A, Yalın OO, Yılmaz IA, Delialioglu N, Yıldız C, Tesdelen B, Kudiaki C. The diagnostic role of serum inflammatory and soluble proteins on dementia subtypes: Correlation with cognitive and functional decline. Behavioural Neurology. 2007; 18(4):207-215.
2. Shah RS, Lee HG, Xiongwei Z, Perry G, Smith MA, Castellani RJ. Current approaches in the treatment of Alzheimer’s disease. Biomedical Pharmacotherapy. 2008 Mar 17.
3. Sascha Weggen, Jason L. Eriksen, Sarah A. Sagi, Claus U. Pietrzik, Victor Ozols, Abdul Fauq, Todd. E. Golde, Edward H. Koo. Evidence that Nonsteroidal Anti-inflammatory Drugs Decrease Ab42 Production by Direct Modulation of g-Secretase Activity. June 12, 2003