TNF is a therapeutic target in Alzheimer's

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Rapid improvement of aphasia and word-finding difficulties, beginning within minutes of administration of an immune molecule, was presented last week at ICAD 2008, the world's leading forum on dementia research. Aphasia means difficulty or inability to use or understand language, causing problems with speech, reading, or writing and interfering with the daily activities of living. Disruption of language function, such as the ability to find words, is a common symptom in advancing Alzheimer's disease, and constitutes an enormous unmet medical need.

This report, also recently published in the Medscape Journal of Medicine, extends and confirms similar findings from a prospective, six month, 12 patient pilot study recently published in BMC Neurology, and additional reports in the Journal of Neuroinflammation and Current Alzheimer Research. Each of these peer-reviewed studies focuses on the effects of perispinal administration of etanercept in dementia. Etanercept is an immune molecule which inactivates excess levels of an immune cytokine called tumor necrosis factor (TNF). This use of perispinal etanercept for dementia and Alzheimer's is beyond the FDA label (off-label). Etanercept is FDA-approved for treating certain forms of arthritis and a skin disorder in both children and adults.

TNF is a critical component of the brain's immune system which finely regulates the transmission of neural impulses between brain cells. The lead author of this study, Edward Tobinick MD, hypothesized that in Alzheimer's and related forms of dementia, such as primary progressive aphasia (PPA), elevated levels of TNF interfere with brain function, and could respond to treatment with perispinal etanercept. Rapid improvement in impaired speech, beginning within minutes, seems to be a unique effect of perispinal etanercept, and illustrates the existence of rapidly reversible TNF-dependent brain mechanisms in Alzheimer's disease and primary progressive aphasia.

Rapid improvement in cognition in patients with Alzheimer's following perispinal etanercept has also been recently reported. These rapid effects are thought to be due to TNF's novel role as a gliotransmitter regulating synaptic transmission (communication between brain cells), a physiologic function of TNF only recently recognized.

These new articles provide further evidence, in addition to accumulating genetic, epidemiologic, and basic science data, that excess TNF is a therapeutic target in Alzheimer's disease and related forms of dementia, and provide an exciting new direction for research. ...http://www.medicalnewstoday.com

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