Directly addressing the hypothesis that systemic inflammation is a driver of dementia is an important priority and, fuelled by the association of elevated serum TNF-α with more rapid cognitive decline [58], the STEADI-09 study (Safety and Tolerability of Etanercept in Alzheimer’s Disease) recently showed that peripheral blocking of TNF-α, using the fusion protein TNF-α inhibitor etanercept, stabilised cognitive function in 20 AD patients with respect to progression in placebo-treated AD patients [105]. The gene discussed is TNF; the disease is Mental deterioration.