Cited by 192Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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Neuronal Hypertrophy in Asymptomatic Alzheimer Disease

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Iacono, Diego, O'Brien, Richard, Resnick, Susan M., Zonderman, Alan B., Pletnikova, Olga, Rudow, Gay, An, Yang, West, Mark J., Crain, Barbara, Troncoso, Juan C.·2008·Journal of Neuropathology & Experimental Neurology

DOI 10.1097/nen.0b013e3181772794PMC PMC2518071

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Abstract

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 Abeta 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 Abeta or tau, or a compensatory mechanism that prevents the progression of the disease into dementia.

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Authors: Iacono, D., O'Brien, R., Resnick, S. M., Zonderman, A. B., Pletnikova, O., Rudow, G., An, Y., West, M. J., Crain, B., & Troncoso, J. C.
Affiliations: Johns Hopkins University (US)
National Institutes of Health (US)
Aarhus University (DK)
Corresponding author: Troncoso, Juan C.
ORCID: Iacono, Diego
Resnick, Susan M.
Zonderman, Alan B.
An, Yang
West, Mark J.
Troncoso, Juan C.
Venue: Journal of Neuropathology & Experimental Neurology
Publisher: Oxford University Press (OUP)
Published: 2008-06
Volume: 67
Issue: 6
Pages: 578-589
ISSN: 0022-3069 (ISSN-L)
1554-6578
DOI: 10.1097/nen.0b013e3181772794
PMC: PMC2518071
OpenAlex: W2097399504
Cited by: 188
References: 67
Citations by year: 2026: 6 · 2025: 16 · 2024: 15 · 2023: 7 · 2022: 11 · 2021: 12 · 2020: 6 · 2019: 14 · 2018: 8 · 2017: 8 · 2016: 11 · 2015: 10 · 2014: 13 · 2013: 17 · 2012: 8
FWCI: 6.09
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Neuropathology & Experimental Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Burroughs Wellcome Fund
Johns Hopkins University
National Institutes of Health
National Institute on Aging (K23AG034550, Z01AG000191, P50AG005146, AG 05146)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: neuronal hypertrophy, hippocampal CA1, anterior cingulate cortex, posterior cingulate cortex, primary visual cortex, mild cognitive impairment, amyloid plaques, neurofibrillary tangles, stereology
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cognition Disorders, Humans, Hypertrophy, Neurons

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Neuronal Hypertrophy in Asymptomatic Alzheimer Disease

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