Cited by 720Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroscience and Neuropharmacology Research

Altered expression of synaptic proteins occurs early during progression of Alzheimer's disease

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Masliah, E., Mallory, M., Alford, M., DeTeresa, R., Hansen, L.A., McKeel, D.W., Morris, J.C.·2001·Neurology

Abstract

The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. Compared with control subjects (CDR = 0), mild (early) AD (CDR = 0.5 to 1) cases had a 25% loss of synaptophysin immunoreactivity. Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins. Thus, synaptic injury in frontal cortex is an early event in AD.

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Crossref · 10.1212/wnl.56.1.127

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  • Synapse loss significantly correlates with cognitive impairment and has been observed to be an early feature of AD pathogenesis.

    “Notably, synapse loss significantly correlates with cognitive impairment [76, 77] and has been observed to be an early feature of AD pathogenesis [78, 79].”
  • Synaptic and neuronal loss developing from senile plaques, neurofibrillary tangles, or other lesions appears critical for the expression of cognitive symptoms.

    “However, SPs and NFTs characterize the neuropathological substrate of AD and synaptic and neuronal loss developing from these or other lesions appear to be critical for the expression of cognitive symptoms.(Masliah et al., 2001; Price et al., 2001)”
  • Senile plaques and neurofibrillary tangles characterize the neuropathological substrate of AD.

    “However, SPs and NFTs characterize the neuropathological substrate of AD and synaptic and neuronal loss developing from these or other lesions appear to be critical for the expression of cognitive symptoms.(Masliah et al., 2001; Price et al., 2001)”

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Research works printed but not linked: 1

  1. Morris JC, Ernesto C, Schaefer K, et al. Clinical dementia rating (CDR) training and reliability protocol: The Alzheimer's Disease Cooperative Study Unit experience. Neurology 1997; 48:1508 -1510.

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Authors
Masliah, E., Mallory, M., Alford, M., DeTeresa, R., Hansen, L. A., McKeel, D. W., & Morris, J. C.
Affiliations
Washington University in St. Louis (US)
Venue
Neurology
Published
2001-01-09
Volume
56
Issue
1
Pages
127-129
ISSN
  • 0028-3878 (ISSN-L)
  • 1526-632X
OpenAlex
W2008767130
Cited by
720
References
10
Citations by year
2026: 15 · 2025: 23 · 2024: 25 · 2023: 29 · 2022: 36 · 2021: 62 · 2020: 28 · 2019: 41 · 2018: 41 · 2017: 37 · 2016: 38 · 2015: 33 · 2014: 46 · 2013: 39 · 2012: 31
FWCI
8.57
Type
journal article
Language
en
Open access
Locations
  • Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (AG10689, AG05131, R01AG010689, P50AG005131, AG 05681, AG13991, P50AG005681)
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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
Alzheimer's disease, synaptic proteins, synaptophysin, synaptotagmin, growth-associated protein 43, synaptic injury, frontal cortex, Clinical Dementia Rating, disease progression, early Alzheimer's disease
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Calcium-Binding Proteins, Frontal Lobe, Humans, Membrane Glycoproteins, Nerve Tissue Proteins, Severity of Illness Index, Synapses, Immunoblotting, Synaptophysin, Disease Progression, GAP-43 Protein, Synaptotagmins

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