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Although there have been meaningful advances in our understanding of Alzheimer disease (AD) pathogenesis, we still do not understand the exact reasons why some individuals develop dementia while others remain normal. This mystery is addressed in this issue of Neurology® by Iacono et al.1 Iacono et al. use sophisticated stereologic techniques to describe morphologic changes in neurons of subjects with asymptomatic AD lesions compared with those who died with mild cognitive impairment (MCI) or cognitively normal individuals with no plaque and tangle pathology. They confirmed that CA1 neurons (and neuronal subparts including the cell body, nucleus, and nucleolus) in subjects with compensated AD lesions (i.e., subjects who were still cognitively normal) were larger than those of control subjects or individuals with MCI, supporting the notion that neuronal hypertrophy in this important hippocampal subregion is associated with a biologic process that protects against cognitive impairment.
Pondering the relationship between neuronal …
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