Jun 162010
 

Readers,

A relationship between vascular risk factors and Alzheimer disease has been considered for over 20 years. In fact, it was widely accepted that “a hardening of the arteries” was to blame for senile dementias. There is also evidence that vascular diseases such as stroke, atherosclerosis, and hypertension are associated with an increased risk of dementia and AD, and that an abnormally elevated level of fibrinogen, the protein critical for blood clot formation, is correlated with AD. Many epidemiologic studies show that practically all of the reported risk factors for AD are related to vascular functions and have an established association with cerebral hypoperfusion.

In the June 10 issue of the journal Neuron, a research team led by Sidney Strickland at Rockefeller University in New York City provides a link between the ß amyloid peptide (Aß) and abnormal fibrin clot formation in cerebral blood vessels. In essence, they suggest a new role for Aß in AD, whereby it would accumulate in the aging brain and interact with fibrinogen. This interaction is thought to lead to persistent clots that obstruct blood flow and engender inflammation. The researchers propose that this altered clotting, compromised blood flow, and inflammation, all contribute to the cognitive decline associated with AD.

This paper nicely establishes a link between fibrin clot formation and Aß protein in animal models of AD, and warrants further investigation, particularly in how this process might occur in the aging human brain.

In the meantime, it should be noted that aerobic exercise (in moderation), has been shown to exert the greatest influence on AD risk reduction, perhaps by optimally affecting cerebral perfusion.

Michael Rafii, MD, PhD
Associate Medical Director, ADCS

Cortes-Canteli M, Paul J, Norris EH, Bronstein R, Ahn HJ, Zamolodchikov D, Bhuvanendran S, Fenz KM, Strickland S. Fibrinogen and ß-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer’s Disease. Neuron. 2010 June 10;66:695-709.

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