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Progress in neurology frequently lags 10 to 20 years behind that of cardiology. Early data correlating cardiovascular disease and serum levels of total and low-density lipoprotein cholesterol have led to treatments (exercise, weight loss, and statins) which have decreased age-adjusted cardiovascular mortality rates by 40%. In this regard, serum cholesterol levels have transitioned from a biomarker to a risk factor as treatment aimed at lowering serum levels have conferred clinical benefits. For 25 years, neurologists have been trying to apply this model to Alzheimer disease (AD) with little success. In the current issue of Neurology,® Ertekin-Taner et al.1 add to the growing literature that plasma Aβ42levels are a potential biomarker for AD.2–6 Because Aβ42 was elevated in plasma in asymptomatic first-degree relatives of patients with presenilin 1, presenilin2, and amyloid precursor protein mutations who had early onset AD (EOAD), they reasoned that Aβ42 levels might also be elevated in asymptomatic first-degree relatives of patients with late onset AD (LOAD).
The Jacksonville Mayo group compared plasma Aβ42 levels between two cohorts of relatives of patients with …
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