New genetic data implicates inflammatory mechanisms in Alzheimer's disease

A front-page article today (April 3, 2011) on the New York Times website reports a new discovery that again implicates inflammatory mechanisms in the pathogenesis of Alzheimer’s disease.

The link is here:…/04alzheimer.html?hp

The article begins:

“New Studies on Alzheimer’s Uncover Genetic Links
Published: April 3, 2011

The two largest studies of Alzheimer’s disease, an international analysis of genes of more than 50,000 people, have led to the discovery of five new genes that make the disease more likely in the elderly and provide tantalizing clues about what might start Alzheimer’s going and fuel its progress in a person’s brain.

The new genes add to a possible theme: so far genes that increase Alzheimer’s risk in the elderly tend to be involved with cholesterol and with inflammation. They also may be used to transport molecules inside cells.

For years, there have been unproven but persistent hints that cholesterol and inflammation are part of the disease process. People with high cholesterol were more likely to get Alzheimer’s disease. In addition, strokes and head injuries, which make Alzheimer’s more likely, also cause brain inflammation….”

The article continues with more discussion. For further background, please consider what is generally known about inflammation and TNF, an immune signaling molecule that is the master regulator of the inflammatory immune response in the human body.

TNF initiates, amplifies, and prolongs the inflammatory response. See the Wikipedia entry:

“Tumor necrosis factor promotes the inflammatory response, which, in turn, causes many of the clinical problems associated with autoimmune disorders such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, hidradenitis suppurativa and refractory asthma. These disorders are sometimes treated by using a TNF inhibitor.”

The NY Times story reports the association of both AD and stroke with inflammatory mechanisms. This association was previously reported in the INR’s recent article in the journal CNS Drugs. In the CNS Drugs article Edward Tobinick MD, Founder of the INR, documented rapid improvement in neurological deficits produced by stroke following the use of the INR’s patented local method of administration of etanercept. Etanercept is a potent biologic antagonist of TNF.

The new Nature Genetics article provides strong new evidence generated by collaborative research from leading Alzheimer research centers that supports the role of inflammatory mechanisms in AD and points to a direction for future research.