Neuronal Hypertrophy in Asymptomatic Alzheimer Disease

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.

doi:10.1097/nen.0b013e3181772794

Cited by 191Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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. +2 more·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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AsymAD individuals have neuritic plaque and NFTs Braak stages at autopsy comparable to those of AD subjects with dementia.
“These individuals have neuritic plaque and NFTs Braak stages at autopsy comparable to those of AD subjects with dementia, and the literature refers to them as resilient [31], Nondemented with AD Neuropathology (NDAN) [83], or asymptomatic AD (AsymAD) [22, 42].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [42]
The Results report that asymptomatic AD (ASYMAD) and dementia-diagnosed AD subjects did not differ significantly in CERAD neuritic plaque classification. They also report a significant difference in Braak NFT staging, so the claim that both measures were comparable is not supported. (LLM, conf=0.94)
Experimental — accuracy not yet measured
AsymAD brains exhibit no signs of notorious synaptic or neuronal deterioration.
“studies have demonstrated that AsymAD brains exhibit no signs of notorious synaptic or neuronal deterioration [8, 42, 73]”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [42]
The Abstract reports neuronal hypertrophy in several regions of ASYMAD brains, supporting a contrast with neuronal shrinkage in those measured cells. But the paper does not establish an absence of neuronal deterioration generally or measure synaptic deterioration; the Introduction discusses possible neuronal and synaptic derangements despite preserved cognition. Page numbers are not available in our copy. (LLM, conf=0.83)
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Editorial [Hot Topic: The Complex and Multifactorial Nature of Alzheimers Disease (Guest Editors: Karim Alkadhi and Jason Eriksen)]
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S1‐02‐01: Neuronal hypertrophy in asymptomatic Alzheimer's disease
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Neuronal hypertrophy in asymptomatic Alzheimer's Disease in the BLSA
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Asymptomatic AD is associated with hypertrophy of CA1‐hippocampus neurons in the NUN study
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P1‐393: Hypertrophy of CA1‐hippocampal neurons and APOE frequency in asymptomatic Alzheimer's disease: Findings from the Nun Study
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Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons
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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
Health Sciences › Medicine › Physiology › 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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