FAQ

Q: Is there independent scientific evidence that TNF as a therapeutic target for Alzheimer’s disease make sense?

A: Yes, and the evidence is coming from multiple academic centers around the world. For example, research presented on November 8, 2010 at the American College of Rheumatology Annual Meeting, entitled  “TNF Inhibition Reduces the Incidence of Alzheimer’s Disease in Rheumatoid Arthritis Patients” found that RA patients taking TNF inhibitors had a 55% reduction in risk of developing AD. This research finding closely followed a November 1 press release from the University of California San Francisco entitled “Arthritis drugs could help prevent memory loss after surgery”. This study, published in the prestigious Proceedings of the National Academy of Sciences found that anti-TNF treatment prevented neuroinflammation and cognitive decline in a basic science model of surgery-induced cognitive decline.

Q: What does this really prove?

A: If one critically looks at these studies, both from reliable and prestigious scientific sources, it will be clear that excess TNF is emerging as a leading therapeutic target in Alzheimer’s Disease. This is exactly what the INR has been saying for years. Moreover, additional recent studies are even more compelling. In a new study entitled “Anti-TNF-alpha reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brains” available online in the journal Brain Research on October 21, 2010, the researchers found anti-TNF treatment in an animal model reduced the levels of TNF, amyloid plaques and tau phosphorylation as early as three days after beginning treatment.