Two new studies, in the Netherlands and Taiwan, suggest that excess levels of TNF (tumor necrosis factor), a protein associated with inflammation, may produce a decline in cognitive functions, i.e., mental tasks involving knowledge, perception, and reasoning. TNF is elevated in the blood in many autoimmune diseases and in the fluid surrounding the brain in Alzheimer's disease.

  The researchers studied cognitive function in patients with either of two autoimmune diseases, rheumatoid arthritis and sarcoidosis. They found that 73.3 percent of the participants in the rheumatoid arthritis study had improvement of cognitive dysfunction after six months of anti-TNF treatment (etanercept, infliximab, or adalimumab). In the sarcoidosis study, patients given anti-TNF treatment were compared with controls. Only patients recently given anti-TNF treatment demonstrated a significant improvement in their score on a standardized cognitive failure questionnaire.

  "These studies suggest that excess TNF may be associated with cognitive decline and that this cognitive dysfunction may respond to anti-TNF treatment," according to Edward Tobinick, M.D., Director of the Institute for Neurological Research, a private medical group, in Los Angeles. "Investigation of TNF-mediated mechanisms may lead to a new understanding of how the immune system influences brain function and may lead to new treatments for a variety of neurological disorders."

--Source: "Cognitive Decline in Alzheimer's and Autoimmune Disease Linked to Common Protein," Institute for Neurological Research, via PR Newswire, June 2, 2010