Cited by 43Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Amyloid load and neural elements in Alzheimer's disease and nondemented individuals with high amyloid plaque density

Mochizuki, Akihide, Peterson, John W., Mufson, Elliott J., Trapp, Bruce D.·1996·Experimental Neurology

Abstract

The amyloid burden and relationship between amyloid deposits and neural elements were investigated in sections of prefrontal neocortex from eight Alzheimer's disease (AD) patients and four age-matched nondemented controls with high amyloid plaque density (HPND). Computer-based image analysis revealed that the total area occupied by betaA4 immunoreactivity was significantly greater (P < 0.031) in AD (27.1%) than in HPND (14.5%) sections. The total betaA4-positive area occupied by nondiffuse plaques was significantly greater (P < 0.05) in AD (13.6%) than in HPND (5.2%) sections. The percentage of diffuse (DPs) and nondiffuse plaques (NDPs) which contained neurons, astrocytes, microglia, dystrophic neurites, and amyloid precursor protein (APP) was also determined. The frequency of association between betaA4 and these neural elements was similar between AD and HPND cases in both diffuse and nondiffuse plaques. Forty percent of DPs in AD and HPND sections contained neuronal perikarya. Microglia, dystrophic neurites, and APP were detected in most nondiffuse plaques in both AD and HPND sections. While astrocyte cell bodies were not present in either diffuse or nondiffuse plaques, their processes were detected in most. These findings indicate that amyloid deposition and nondiffuse plaques are greater in AD than in HPND sections. The association between microglia and nondiffuse plaques supports the hypothesis that these resident immune cells participate in aggregation and redistribution of amyloid deposits and possibly formation of dystrophic neurites.

Integrity signals

Registry

Crossref · 10.1006/exnr.1996.0181

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Still being checked.

Cited by

Sorted by citations

Authors
Mochizuki, A., Peterson, J. W., Mufson, E. J., & Trapp, B. D.
Affiliations
  • Cleveland Clinic (US)
  • Rush University Medical Center (US)
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
1996-11
Volume
142
Issue
1
Pages
89-102
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2010694299
Cited by
43
References
0
Citations by year
2025: 1 · 2021: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 1 · 2012: 4
FWCI
0.67
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns030451-05)
  • National Institute on Aging (AG 10161, AG09466, P30AG010161, P01AG009466)
  • National Institute of Neurological Disorders and Stroke (NS 30451)
Topics
  • Health Sciences › Medicine › Physiology › 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, amyloid plaques, amyloid-beta, prefrontal cortex, diffuse plaques, microglia, astrocytes, dystrophic neurites, amyloid precursor protein, neuronal perikarya, amyloid deposition
MeSH terms
Age Factors, Aged, Aged, 80 and over, Aging, Alzheimer Disease, Astrocytes, Female, Humans, Male, Middle Aged, Neurons, Amyloid beta-Protein Precursor, Prefrontal Cortex, Microglia

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review