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Editorials |

Treat Alzheimer Disease Before It Is Symptomatic

Roger N. Rosenberg, MD, Editor
Arch Neurol. 2011;68(10):1237-1238. doi:10.1001/archneurol.2011.135.
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In this issue of the Archives, Lo et al1 describe longitudinal changes in cerebrospinal fluid (CSF) β-amyloid 42 (Aβ42), fludeoxyglucose–positron emission tomography, and magnetic resonance imaging hippocampal volume and associated cognitive loss in normal aging, mild cognitive impairment (MCI), and Alzheimer disease (AD). The trajectories of these biomarkers, they find, vary across different cognitive stages. Their findings show that CSF Aβ42 declines prior to the beginning of cognitive loss. Glucose metabolism measuring neuronal dysfunction falls next, followed by neuronal injury and loss as defined by hippocampal atrophy. Their data provide compelling evidence that amyloid deposition occurs early in the disease process, before hypometabolism or hippocampal atrophy, “suggesting that biomarker prediction for cognitive change is stage dependent.” Their study is in agreement with that of Jack et al,2 expressing the view that Aβ42 deposition leading to formation of Aβ plaques occurs while individuals are still cognitively normal, leading after a lag period to neuronal dysfunction, metabolic impairment, and neurodegeneration with neuronal loss and brain atrophy.

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