Two new studies suggest that excess levels of a protein associated with inflammation, TNF, may produce cognitive decline. TNF regulates both inflammation and brain function. TNF is elevated in the blood in many autoimmune diseases, and in the fluid surrounding the brain in Alzheimer's disease.
The new studies, from medical centers in Taiwan and the Netherlands, examined cognitive function in patients with either of two autoimmune diseases, rheumatoid arthritis (RA) and sarcoidosis, after 6 months of treatment with an anti-TNF therapeutic (etanercept, infliximab, or adalimumab). 73.3% of the participants in the RA study had amelioration of cognitive dysfunction after 6 months of anti-TNF treatment ). 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 new results are concordant with previous reports of sustained cognitive improvement following the initiation of anti-TNF treatment in Alzheimer's disease.
"These studies suggest that TNF-induced cognitive dysfunction may be operative in a diverse group of inflammatory diseases and provide further support for investigating anti-TNF treatment for Alzheimer's disease," commented Edward Tobinick MD, Director of the Institute for Neurological Research®(INR®), a private medical group, inc. in Los Angeles. Specific patented anti-TNF treatment methods in neurology invented by Dr. Tobinick are the subject of a new scientific review.
"These studies all suggest that excess TNF may be associated with cognitive decline, and that this cognitive dysfunction may respond to anti-TNF treatment. 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."
Institute for Neurological Research, a private medical group, inc.