The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Quantitation of cerebral atrophy in preclinical and end-stage Alzheimer’s disease
Abstract
Morphometric analysis of standardized gross cerebral slices from 16 patients with end-stage Alzheimer's disease (AD), 14 controls without neuropathological lesions or neurological disease, and 4 neurologically intact nondemented patients with histopathological lesions of AD was used to measure cross-sectional areas of cerebral cortex, white matter, subcortical nuclei, and the ventricular system. In AD, there was global cerebral atrophy of both cortex and white matter, selective atrophy of the amygdala and hippocampus, and ex vacuo hydrocephalus. In addition, in half the cases of AD, white matter atrophy was associated with overt histopathological evidence of patchy rarefaction of fibers and gliosis. Patients with preclinical AD had prominent and selective shrinkage of white matter comparable to that observed in AD, yet their cortical areas were normal. These observations suggest that white matter degeneration is an intrinsic component of AD. Moreover, its presence in preclinical AD where cortical atrophy is not evident indicates that cytoskeletal abnormalities associated with axonal degeneration may precede and perhaps cause the cortical atrophy observed in clinically manifested AD.
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“However, previous neuroimaging as well as post-mortem brain studies have observed white matter alterations in the presence of minimal or only weak grey matter atrophy (de la Monte, 1989; Zhuang et al., 2012), suggesting that in principle white matter alterations in Alzheimer’s disease are not dependent on grey matter atrophy.”
From White matter diffusion alterations precede symptom onset in autosomal dominant Alzheimer’s disease (2018) · cites this paper as de la Monte, 1989
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Metadata
- Authors
- de la Monte, S. M.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1989-05
- Volume
- 25
- Issue
- 5
- Pages
- 450-459
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2062125611
- Cited by
- 229
- References
- 33
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 8 · 2022: 2 · 2021: 5 · 2020: 6 · 2019: 8 · 2018: 12 · 2017: 7 · 2016: 9 · 2015: 6 · 2014: 8 · 2013: 10 · 2012: 9
- FWCI
- 8.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG05134-03)
- 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
- Alzheimer's disease, brain atrophy, preclinical Alzheimer's disease, white matter atrophy, cortical atrophy, hippocampal atrophy, amygdala atrophy, gliosis, axonal degeneration, cytoskeletal abnormalities, brain ventricles, subcortical nuclei
- MeSH terms
- Alzheimer Disease, Atrophy, Humans
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