Synapse loss in dementias
Open accessAbstract
Synaptic transmission is essential for nervous system function, and its dysfunction is a known major contributing factor to Alzheimer's‐type dementia. Antigen‐specific immunochemical methods are able to characterize synapse loss in dementia through the quantification of various synaptic proteins involved in the synaptic cycle. These immunochemical methods applied to the study of Alzheimer's disease (AD) brain specimens have correlated synaptic loss with particularly toxic forms of amyloid‐β protein and have also established synapse loss as the best correlate of dementia severity. A significant but comparatively circumscribed amount of literature describes synaptic decline in other forms of dementia. Ischemic vascular dementia (IVD) is quite heterogeneous, and synapse loss in IVD seems to be variable among IVD subtypes, probably reflecting its variable neuropathologic correlates. Loss of synaptic protein has been identified in vascular dementia of the Binswanger type and Spatz‐Lindenberg's disease. Here we demonstrate a significant loss of synaptophysin density within the temporal lobe of frontotemporal dementia (FTD) patients. © 2010 Wiley‐Liss, Inc.
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These tau changes correlate with degeneration of synapses and neuronal loss in frontal and temporal cortices.
“These changes correlate with degeneration of synapses and neuronal loss in frontal and temporal cortices (Bodea et al., 2016; Clare et al., 2010).”
From ELAVL4, splicing, and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids (2021) · cites this paper as Clare et al., 2010
The ‘Synaptic Proteins and AD’ section reports a correlation between synapse loss and neurons containing neurofibrillary tangles, but also notes that another synaptic marker showed no correlation with tangle density. The FTLD section reports synaptic reductions in frontal and temporal regions. Neither section establishes that tau changes correlate with neuronal loss in those cortices. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPathologic studies reveal accumulation of filamentous, hyperphosphorylated tau protein in cerebral cortical and hippocampal neurons and glia, and tau redistribution from axons to the somatodendritic compartment.
“Pathologic studies reveal accumulation of filamentous, hyperphosphorylated tau protein (P-tau) in cerebral cortical and hippocampal neurons and glia, and tau redistribution from axons to the somatodendritic compartment.”
From ELAVL4, splicing, and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids (2021) · cites this paper as Clare et al., 2010
The 'Synaptic Proteins and AD' section mentions neurons containing neurofibrillary tangles, but does not identify their composition or describe tau pathology. Searches for hyperphosphorylated tau and its redistribution from axons to the somatodendritic compartment found no passage addressing the claim in our copy; page numbers were unavailable. (LLM, conf=0.72)
Experimental — accuracy not yet measuredThe pathological interplay between loss of synaptic functionality and neurodegeneration remains poorly understood.
“However, the pathological interplay between loss of synaptic functionality and neurodegeneration remains poorly understood [14].”
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References 61 · Cited by 163
- Authors
- Clare, R., King, V. G., Wirenfeldt, M., & Vinters, H. V.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Wirenfeldt, Martin
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2010-06-07
- Volume
- 88
- Issue
- 10
- Pages
- 2083-2090
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- PMC
- PMC3068914
- OpenAlex
- W2007804566
- Cited by
- 163
- References
- 61
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 14 · 2023: 11 · 2022: 28 · 2021: 19 · 2020: 10 · 2019: 9 · 2018: 11 · 2017: 9 · 2016: 5 · 2015: 7 · 2014: 7 · 2013: 11 · 2012: 5
- FWCI
- 0.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Forsknings- og Innovationsstyrelsen
- Danish Agency for Science and Higher Education
- National Institute on Aging (AG 12435, P50AG016570, P50-AG 16570, P01AG012435)
- 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
- synaptic loss, Alzheimer's disease, vascular dementia, frontotemporal dementia, synaptophysin, amyloid-beta, synaptic proteins, dementia severity, Binswanger disease, temporal lobe
- MeSH terms
- Animals, Brain, Dementia, Humans, Synapses
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