Cited by 476Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.

Deficient glutamate tranport is associated with neurodegeneration in Alzheimer's disease

Abstract

The mechanisms of synapse damage in Alzheimer's disease (AD) are not fully understood. Deficient functioning of glutamate transporters might be involved in synaptic pathology and neurodegeneration by failing to clear excess glutamate at the synaptic cleft. In AD, glutamate transporter activity as assessed by D-[3H]aspartate binding is decreased; however, it is not clear to what extent it is associated with the neurodegenerative process and cognitive alterations. For this purpose, levels of D- and L-[3H]aspartate binding in midfrontal cortex were correlated with synaptophysin levels, brain spectrin degradation product levels, and clinical and neuropathological indicators of AD. Compared to control brains, AD brains displayed a 34% decrease in levels of D-[3H]aspartate binding, a 30% decrease in L-[3H]aspartate binding, and a 48% loss of synaptophysin immunoreactivity. Increased levels of brain spectrin degradation products correlated with a decrease in levels of D-[3H] and L-[3H]aspartate binding, and decreased levels of synaptophysin immunoreactivity. Levels of L-[3H]aspartate binding correlated with levels of synaptophysin immunoreactivity. These results suggest that decreased glutamate transporter activity in AD is associated with increased excitotoxicity and neurodegeneration, supporting the possibility that abnormal functioning of this system might be involved in the pathogenesis of synaptic damage in AD.

Overview

Integrity signals

Registry

Crossref · 10.1002/ana.410400512

Cites

73 of 73 references verified0 citation errors · 0 not checkable

Statistics

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

Verification

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?

Citations

Cites

Research works printed but not linked: 6

  1. Masliah E, 1994, The role of synaptic pathology in the mechanisms of dementia in Alzheimer's disease, Clin Neurosci, 1, 192
  2. Hof PR, 1994, Alzheimer disease, 197
  3. Palmer AM, 1990, Is the neuronal basis of Alzheimer's disease cholinergic or glutamaterigc?, FASEB J, 2745, 2752
  4. Masliah E, 1995, Abnormal synaptic regeneration in hAPP695 transgenic and APOE knockout mice, 405
  5. Greenamyre JT, 1994, Anatomy and physiology of lgutamate in the CNS, Neurology, 44, S7
  6. 10.1002/ana.410380114 · DOI · Paper page

Cited by

Sorted by citations

See all 476

Metadata

Authors
Masliah, E., Hansen, L., Alford, M., Deteresa, R., & Mallory, M.
Affiliations
University of California San Diego (US)
Corresponding author
Masliah, E.
Venue
Annals of Neurology
Publisher
Wiley
Published
1996-11
Volume
40
Issue
5
Pages
759-766
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
OpenAlex
W2050523782
Cited by
476
References
73
Citations by year
2026: 13 · 2025: 17 · 2024: 20 · 2023: 17 · 2022: 27 · 2021: 21 · 2020: 24 · 2019: 32 · 2018: 24 · 2017: 17 · 2016: 11 · 2015: 20 · 2014: 13 · 2013: 10 · 2012: 12
FWCI
6.74
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (AG10689, AG05131, R01AG010689, P50AG005131)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, glutamate transporters, excitotoxicity, neurodegeneration, synapse damage, synaptophysin, synaptic pathology
MeSH terms
Aged, Aspartic Acid, Autopsy, Biological Transport, Brain, Frontal Lobe, Humans, Nerve Degeneration, Organ Specificity, Reference Values, Regression Analysis, Spectrin, Biomarkers, Synaptophysin, Neurofibrillary Tangles, ATP-Binding Cassette Transporters, Amino Acid Transport System X-AG

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