Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 67, Issue 6, Pages 578-589Publisher
OXFORD UNIV PRESS INC
DOI: 10.1097/NEN.0b013e3181772794
Keywords
beta-amyloid; Alzheimer disease pathogenesis; mild cognitive impairment; nuclear hypertrophy; nucleolar hypertrophy; neuronal resistance; tau
Categories
Funding
- Intramural NIH HHS [Z01 AG000191-11] Funding Source: Medline
- NIA NIH HHS [K23 AG034550, AG05146, P50 AG005146-25, P50 AG005146] Funding Source: Medline
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The pathologic changes of Alzheimer disease (AD) evolve very gradually over decades before the disease becomes clinically manifest. Thus, it is not uncommon to find substantial numbers of A beta plaques and neurofibrillary tangles in autopsy brains of older subjects with documented normal cognition, a state that we define as asymptomatic AD (ASYMAD). The goal of this study is to understand the morphometric substrate of ASYMAD subjects compared with mild cognitive impairment and definite AD cases. We used designed-based stereology to measure the volumes of neuronal cell bodies, nuclei, and nucleoli in 4 cerebral regions: anterior cingulate gyrus, posterior cingulate gyrus, primary visual cortex, and CA1 of hippocampus. We examined and compared autopsy brains from 4 groups (n = 15 each) of participants in the Baltimore Longitudinal Study of Aging: ASYMAD, mild cognitive impairment, AD, and age-matched controls. We found significant hypertrophy of the neuronal cell bodies, nuclei, and nucleoli of CA1 of hippocampus and anterior cingulate gyrus neurons in ASYMAD subjects compared with control and mild cognitive impairment cases. In the posterior cingulate gyrus and primary visual cortex, the hypertrophy was limited to the nuclei and nucleoli. The hypertrophy of cortical neurons and their nuclei and nucleoli in ASYMAD may represent an early reaction to the presence of neurotoxic A beta or tau, or a compensatory mechanism that prevents the progression of the disease into dementia.
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