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To the Editor:
I commend Tan et al.,1 whose excellent study provides substantial scientific support for the inflammatory hypothesis of Alzheimer disease (AD) and specifically suggests that patients whose peripheral blood mononuclear cells produce higher levels of the proinflammatory cytokine TNF-alpha may have an increased AD risk.
The authors have avoided the necessity of taking serial CSF samples by using a surrogate marker of TNF-alpha, its production by peripheral blood mononuclear cells. This technique may have traversed the fact that large molecules such as TNF-alpha have difficulty in crossing the blood–brain barrier, although in the case of TNF-alpha there may be a modest degree of crossing due to the existence of active transport mechanisms.2
This study joins an increasing body of scientific evidence implicating excess TNF-alpha in the pathogenesis of AD, which now includes robust genetic evidence, new basic science data, and a pilot study examining the effect of a novel method of administration of the anti-TNF biologic, etanercept, in AD.3,4 A new study suggests that CNS synaptic function may be subject to regulation by the immune system, including TNF-alpha.5 It is possible that if excess TNF-alpha is present in the brain in AD (a fact which is not established, but only suggested by the present study), the excess TNF-alpha may contribute to the synaptic dysfunction that may …
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