The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Synaptic and neuritic alterations during the progression of Alzheimer's disease
Abstract
Extensive synaptic and neuritic alterations in the neocortex and limbic system are characteristically found in Alzheimer's disease (AD). However, it is not known how early in the development of the disease these alterations occur. For the present study, we compared the synaptic and neuritic alterations among cases classified clinically and neuropathologically as early, mild and advanced AD. In early AD there was a 20% loss of synaptophysin-immunoreactive presynaptic terminals in the outer molecular layer of the hippocampal dentate gyrus (but not in the neocortex and entorhinal cortex), accompanied by increased amyloid precursor protein (APP) and Alz50 immunoreactivity in hippocampal and entorhinal cortex pyramidal neurons. These results suggest that abnormal neuronal expression of APP and cytoskeletal proteins in early stages might be involved in the mechanisms of synaptic pathology in AD.
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In the citing paper
“which may be a result of our focus on the earliest stages of pathology and/or a dissociation between plaque load and function, which has been observed in other settings.21,60,62”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [21]
In the citing paper
“Remarkably, APP mutant neurons showed differential alterations in synaptic proteins [3] that resembled those that have been described in AD brain, such as early loss of the pre-synaptic protein synaptophysin [113, 163, 192] and the post-synaptic protein PSD-95 [63].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [113]
Citations
Cites
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Self-citationNeurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease
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Self-citationPerforant pathway changes and the memory impairment of Alzheimer's disease
Hyman, B. T., Van Hoesen, G. W., Kromer, L. J., & Damasio, A. R. (1986) · Annals of Neurology · doi:10.1002/ana.410200406 · Cited by 672
Identification of normal and pathological aging in prospectively studied nondemented elderly humans
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Cited by
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Neuropathological alterations in Alzheimer disease
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006189 · Cited by 3,345
Self-citationMucke, L., Masliah, E., Yu, G.-Q., Mallory, M., Rockenstein, E. M., Tatsuno, G., Hu, K., Kholodenko, D., Johnson-Wood, K., & McConlogue, L. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04050.2000 · Cited by 1,856
Self-citationBeta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red.
Lorenzo, A., & Yankner, B. A. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.25.12243 · Cited by 1,324
The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
Spires-Jones, T. L., & Hyman, B. T. (2014) · Neuron · doi:10.1016/j.neuron.2014.05.004 · Cited by 1,201
A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease
Tuszynski, M. H., Thal, L., Pay, M., Salmon, D. P., U, H. S., Bakay, R., Patel, P., Blesch, A., Vahlsing, H. L., Ho, G., et al. (2005) · Nature Medicine · doi:10.1038/nm1239 · Cited by 1,050
Self-citation
Metadata
- Authors
- Masliah, E., Mallory, M., Hansen, L., Richard, D., Alford, M., & Terry, R.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Masliah, Eliezer
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1994-06
- Volume
- 174
- Issue
- 1
- Pages
- 67-72
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2073518622
- Cited by
- 370
- References
- 30
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 10 · 2023: 17 · 2022: 12 · 2021: 15 · 2020: 19 · 2019: 15 · 2018: 15 · 2017: 11 · 2016: 10 · 2015: 14 · 2014: 11 · 2013: 15 · 2012: 18
- FWCI
- 4.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag008205-08, 5r01ag008201-05)
- National Institute on Aging (AG 08205, AG05131, P50AG005131, AG08201)
- 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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, synaptic pathology, synaptophysin, presynaptic terminals, amyloid precursor protein, amyloid plaques, dentate gyrus, entorhinal cortex, hippocampus, pyramidal neurons, cytoskeletal proteins, disease progression
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Amyloid, Cerebral Cortex, Cytoskeleton, Hippocampus, Humans, Nerve Tissue Proteins, Synapses, Neurites, Synaptophysin, Pyramidal Cells, Entorhinal Cortex
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