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Cited by 79Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Soluble amyloid beta levels are elevated in the white matter of Alzheimer’s patients, independent of cortical plaque severity

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Collins-Praino, Lyndsey E, Francis, Yitshak I, Griffith, Erica Y, Wiegman, Anne F, Urbach, Jonathan, Lawton, Arlene, Honig, Lawrence S, Cortes, Etty, Vonsattel, Jean Paul G, Canoll, Peter D, Goldman, James E, Brickman, Adam M·2014·Acta Neuropathologica Communications
DOI 10.1186/s40478-014-0083-0PMC PMC4147157
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Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease and the leading cause of dementia. In addition to grey matter pathology, white matter changes are now recognized as an important pathological feature in the emergence of the disease. Despite growing recognition of the importance of white matter abnormalities in the pathogenesis of AD, the causes of white matter degeneration are still unknown. While multiple studies propose Wallerian-like degeneration as the source of white matter change, others suggest that primary white matter pathology may be due, at least in part, to other mechanisms, including local effects of toxic Aβ peptides. In the current study, we investigated levels of soluble amyloid-beta (Aβ) in white matter of AD patients (n=12) compared with controls (n=10). Fresh frozen white matter samples were obtained from anterior (Brodmann area 9) and posterior (Brodmann area 1, 2 and 3) areas of post-mortem AD and control brains. ELISA was used to examine levels of soluble Aβ -42 and Aβ -40. Total cortical neuritic plaque severity rating was derived from individual ratings in the following areas of cortex: mid-frontal, superior temporal, pre-central, inferior parietal, hippocampus (CA1), subiculum, entorhinal cortex, transentorhinal cortex, inferior temporal, amygdala and basal forebrain. Compared with controls, AD samples had higher white matter levels of both soluble Aβ -42 and Aβ -40. While no regional white matter differences were found in Aβ -40, Aβ -42 levels were higher in anterior regions than in posterior regions across both groups. After statistically controlling for total cortical neuritic plaque severity, differences in both soluble Aβ -42 and Aβ -40 between the groups remained, suggesting that white matter Aβ peptides accumulate independent of overall grey matter fibrillar amyloid pathology and are not simply a reflection of overall amyloid burden. These results shed light on one potential mechanism through which white matter degeneration may occur in AD. Given that white matter degeneration may be an early marker of disease, preceding grey matter atrophy, understanding the mechanisms and risk factors that may lead to white matter loss could help to identify those at high risk and to intervene earlier in the pathogenic process.

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Metadata

Authors
Collins-Praino, L. E., Francis, Y. I., Griffith, E. Y., Wiegman, A. F., Urbach, J., Lawton, A., Honig, L. S., Cortes, E., Vonsattel, J. P. G., Canoll, P. D., Goldman, J. E., & Brickman, A. M.
Affiliations
Columbia University (US)
Corresponding author
Brickman, Adam M
ORCID
Venue
Acta Neuropathologica Communications
Publisher
Springer Science and Business Media LLC
Published
2014-08-17
Volume
2
Issue
1
Pages
83-83
ISSN
2051-5960 (ISSN-L)
DOI
10.1186/s40478-014-0083-0
PMC
PMC4147157
OpenAlex
W2096766291
Cited by
79
References
76
Citations by year
2026: 3 · 2025: 5 · 2024: 7 · 2023: 10 · 2022: 2 · 2021: 10 · 2020: 13 · 2019: 9 · 2018: 10 · 2017: 3 · 2016: 4 · 2015: 2
FWCI
2.00
Type
journal article
Language
en
Open access
Licence
Locations
  • Acta Neuropathologica Communications (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion, cc-by)
  • Columbia Academic Commons (Columbia University)
Funders
  • Alzheimer's Association (AG034189, P50 AG008702)
  • Mary E. Groff Surgical and Medical Research and Education Charitable Trust
  • National Institutes of Health (AG034189, AG008702)
  • National Institute on Aging (R01AG034189, P50AG008702)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, soluble amyloid-beta, white matter degeneration, amyloid-beta 42, Aβ40, neuritic plaques, postmortem brain, amyloid burden
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Cerebral Cortex, Female, Humans, Male, Amyloid beta-Peptides, Plaque, Amyloid, White Matter

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