Excess levels of TNF immune signaling protein key factor in AD

Three new studies provide converging evidence pointing to a new therapeutic target in Alzheimer's Disease(AD). These studies, from independent academic centers in the U.S., England, and China, point to excess levels of a protein called TNF as a key factor in AD. TNF is an immune signaling protein that regulates both inflammation and neuronal communication in the brain. As a target it is radically different from the amyloid plaques that have been the main focus of AD research for two decades. The new studies suggest the promise of a wholly new way to treat AD.

The latest study, to be presented at the Annual Meeting of the American College of Rheumatology this week, reports a 55% reduction in risk of developing Alzheimer's dementia for rheumatoid arthritis patients who received anti-TNF treatment compared with controls. The study, entitled "Tumor Necrosis Factor Inhibition Reduces the Incidence of Alzheimer's Disease in Rheumatoid Arthritis Patients" involved a review of the medical and pharmacy claims of 42,193 patients with a pre-existing diagnosis of RA. 165 patients with AD (cases) were matched to 1,393 controls in this nested case-control study. In this population of adults with RA the risk of AD was reduced by TNF inhibitor therapy, but not by other disease modifying agents used for treatment of RA. The authors concluded that TNF may be an important component in the pathogenesis of AD. The study was a collaboration between researchers from Dartmouth Medical School, Massachusetts General Hospital, Verisk Health, and Harvard Medical School.

The ACR study closely follows on the heels of a study published November 1 in the Proceedings of the National Academy of Sciences entitled "Tumor necrosis factor-alpha triggers a cytokine cascade yielding postoperative cognitive decline". In this collaboration of the Imperial College and Kennedy Institute of Rheumatology in London and UCSF, anti-TNF treatment was found to prevent neuroinflammation and cognitive decline in an animal model of surgery-induced cognitive decline. This study provided further evidence that TNF, widely recognized as playing a key role in arthritis, may also play a key role in cognitive disorders associated with inflammation.

Just prior to publication of the PNAS study researchers from Nanjing Medical University in China reported that anti-TNF treatment reduced the levels of TNF, amyloid plaques and tau phosphorylation in an animal model, surprisingly as early as three days after beginning treatment. (Brain Research, accepted manuscript published online October 21 entitled "Anti-TNF-alpha reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brains"). The authors of the Brain Research manuscript concluded that their results support the use of anti-TNF for treatment of AD.

Anatomically targeted anti-TNF treatment for Alzheimer's disease was invented by Edward Tobinick MD, Medical Director of the INR® in Los Angeles.  See: Tumour necrosis factor modulation for treatment of Alzheimer's disease: rationale and current evidence. Edward Tobinick MD. CNS Drugs. 2009 Sep 1;23(9):713-25. For further information, please see the website of the INR, at http://www.nrimed.com. Anatomically targeted anti-TNF treatment for Alzheimer's disease is a patented invention of the INR; U.S. patents 6982089; 7214658; 7629311; Australia patent 758523 and other issued and pending patents assigned to TACT IP, LLC.

Source:

Institute for Neurological Research

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