01 May 2012


Neuro Review Article of Alzheimer’s disease

ALZHEIMER’S DISEASE AND INFLAMMATION:  A REVIEW OF CELLULAR AND THERAPEUTIC MECHANISMS

Alzheimer’s disease is the fourth leading cause of death in persons over the age of 65.  It is incurable and progressive and affects millions of people across the world.  Alzheimer’s disease (AD) is the most common neurodegenerative disease that causes dementia.  The three major pathological hallmarks of this disease are characterized as senile plaques, neurofibrillary tangles, and inflammation.  Senile plaques consist primarily of protein deposits, namely b-amyloid fragments.  These amyloid fragments seem to mediate inflammatory mechanisms by activating microglial cells via the complement pathway in a similar fashion to immunoglobulins.  Platelets are a major source of amyloid fragments thus therapies are proposed to curve platelet numbers and thus a source of protein fragments.  Also the use of NSAIDS to reduce the inflammatory microglial cell activation is discussed.

Inflammation of neuronal tissue can both be beneficial and detrimental depending on circumstances.  For example in brain injury the inflammatory response can:  aid in clearing out dead cells, debris, inhibit neuro toxic cytokines, and promote growth factors needed for recovery.  Conversely improper or chronic inflammation can cause severe damage and widespread death of neuronal cells worsening prognosis.  Possible drug interventions to curve these deleterious effects are proposed.  Evidence from RA patients who consume anti-inflammatory medications regularly does seem to show slowing of the progression of AD.  In conclusion the author’s call for future studies aimed at targeting the inflammatory process via NSAIDS and anti-platelet therapies. 



Source:  Glenda Halliday,* Stephen R Robinson,‡ Claire Shepherd* and Jillian Kril.  BRIEF REVIEW:  ALZHEIMER’S DISEASE AND INFLAMMATION: A REVIEW OF CELLULAR AND THERAPEUTIC MECHANISMS, Clinical and Experimental Pharmacology and Physiology (2000) 27, 1–8.

1 comment:

  1. This is a really interesting concept, but definitely carries some of those risk/benefit stipulations we have been talking about this semester. Like you mentioned Mike, the people who have the reduced progression of AD are already using NSAIDs on a regular basis to manage their rheumatoid arthritis. What I really end up wondering is how often and how early on would a person have to start taking anti-inflammatory medication in order to slow the disease, especially when considering the downsides to NSAIDs. Like we talked about in class, using this medication comes with an increased cardiovascular risk. I think it would be really cool to see a specific study of the effects of NSAID use on the pathology and physiological development of AD.

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