Synaptic Changes in Alzheimer's Disease
Open accessAbstract
In an effort to examine changes that precede synapse loss, we have measured amyloid-beta and a series of damage markers in the synaptic compartment of Alzheimer's disease (AD) cases. Because localization of events to the terminal region in neurons is problematic with conventional methods, we prepared synaptosomes from samples of cryopreserved human association cortex, and immunolabeled terminals with a procedure for intracellular antigens. Fluorescence was quantified using flow cytometry. The viability dye calcein AM was unchanged in AD terminals compared to controls, and the fraction of large synaptosome particles did not change, although a striking loss of large terminals was observed in some AD cases. The percent positive fraction for a series of pre- and postsynaptic markers was not affected by AD in this cohort. However, the amyloid-beta-positive fraction increased from 16 to 27% (P < 0.02) in terminals from AD cortex. The expression level on a per-terminal basis is indicated in this assay by fluorescence (relative fluorescence units). The fluorescence of presynaptic markers did not change in AD terminals, but PSD-95 fluorescence was decreased by 19% (P < 0.03). Amyloid-beta fluorescence was increased by 132% (P < 0.01), and glial fibrillary acidic protein labeling by 31% (P < 0.01). These results suggest that synapse-associated amyloid-beta is prominent in regions relatively unaffected by AD lesions, and that amyloid accumulation in surviving terminals is accompanied by gliosis and alteration in the postsynaptic structure.
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APP mutant neurons show differential alterations in synaptic proteins resembling those in AD brain, including early loss of synaptophysin and PSD-95.
“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 [63]
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- Authors
- Gylys, K. H., Fein, J. A., Yang, F., Wiley, D. J., Miller, C. A., & Cole, G. M.
- Affiliations
- University of California, Los Angeles (US)
- University of Southern California (US)
- Corresponding author
- Gylys, Karen Hoppens
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2004-11
- Volume
- 165
- Issue
- 5
- Pages
- 1809-1817
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1618663
- OpenAlex
- W2135224381
- Cited by
- 253
- References
- 59
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 13 · 2023: 9 · 2022: 9 · 2021: 10 · 2020: 13 · 2019: 9 · 2018: 11 · 2017: 14 · 2016: 11 · 2015: 13 · 2014: 21 · 2013: 13 · 2012: 11
- FWCI
- 4.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AI28697, CA16042)
- National Institute on Aging (AG18879, R01AG018879, P50AG016570, R01AG013741, AG 16570, P50-AG05142, P50AG005142, AG13741)
- National Cancer Institute (CA-16 042, P30CA016042)
- National Institute of Allergy and Infectious Diseases (AI-28 697, P30AI028697)
- Topics
- Health Sciences › Medicine › Physiology › 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, synaptic loss, amyloid-beta, synaptosomes, synapses, PSD-95, postsynaptic structures, presynaptic terminals, glial fibrillary acidic protein, gliosis, association cortex
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Flow Cytometry, Glial Fibrillary Acidic Protein, Gliosis, Humans, Male, Membrane Proteins, Models, Biological, Nerve Tissue Proteins, Neurons, Synapses, Time Factors, Blotting, Western, Amyloid beta-Peptides, Synaptosomal-Associated Protein 25
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