Synapses and Alzheimer's Disease

Sheng, M.; Sabatini, B. L.; Sudhof, T. C.

doi:10.1101/cshperspect.a005777

Cited by 441Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

Synapses and Alzheimer's Disease

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Sheng, M., Sabatini, B. L., Sudhof, T. C.·2012·Cold Spring Harbor Perspectives in Biology

DOI 10.1101/cshperspect.a005777PMC PMC3331702

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Abstract

Alzheimer's disease (AD) is a major cause of dementia in the elderly. Pathologically, AD is characterized by the accumulation of insoluble aggregates of Aβ-peptides that are proteolytic cleavage products of the amyloid-β precursor protein ("plaques") and by insoluble filaments composed of hyperphosphorylated tau protein ("tangles"). Familial forms of AD often display increased production of Aβ peptides and/or altered activity of presenilins, the catalytic subunits of γ-secretase that produce Aβ peptides. Although the pathogenesis of AD remains unclear, recent studies have highlighted two major themes that are likely important. First, oligomeric Aβ species have strong detrimental effects on synapse function and structure, particularly on the postsynaptic side. Second, decreased presenilin function impairs synaptic transmission and promotes neurodegeneration. The mechanisms underlying these processes are beginning to be elucidated, and, although their relevance to AD remains debated, understanding these processes will likely allow new therapeutic avenues to AD.

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Previous studies using transgenic mouse models of AD have identified various mechanisms that lead to synaptic impairment in AD, including the accumulation of soluble amyloid-beta, Tau hyperphosphorylation, loss of VGF signaling, and glial state dysregulation.
“For example, previous studies using transgenic mouse models of AD have identified various mechanisms that lead to synaptic impairment in AD, including the accumulation of soluble amyloid-beta, Tau hyperphosphorylation, loss of VGF signaling, and glial state dysregulation (e.g., the induction of disease-associated microglia and disease-associated astrocytes) (9, 23–30).”
From Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer’s disease (2020) · cites this paper as [24]

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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“The most recent version of the amyloid hypothesis (or Ab hypothesis) suggests that AD arises from synaptic toxicity mediated bysoluble microaggregates (also termed oligomers) of Ab, leading to synaptic dysfunction and synapse loss (“synapse failure”) (Lambert et al. 1998; Selkoe 2002; Kamenetz et al. 2003; Cleary et a…”
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The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
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Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies
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Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer’s disease
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Meta‐analysis of synaptic pathology in Alzheimer's disease reveals selective molecular vesicular machinery vulnerability
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Hémar, A., & Mulle, C. (2011) · médecine/sciences · doi:10.1051/medsci/2011278015 · Cited by 8 · see citing works

Authors: Sheng, M., Sabatini, B. L., & Sudhof, T. C.
Affiliations: Genentech (US)
Howard Hughes Medical Institute (US)
Corresponding author: Sheng, M.
ORCID: Sheng, M.
Sabatini, B. L.
Venue: Cold Spring Harbor Perspectives in Biology
Publisher: Cold Spring Harbor Laboratory
Published: 2012-04-04
Volume: 4
Issue: 5
Pages: a005777-a005777
ISSN: 1943-0264 (ISSN-L)
DOI: 10.1101/cshperspect.a005777
PMC: PMC3331702
OpenAlex: W2120551490
Cited by: 436
References: 134
Citations by year: 2026: 21 · 2025: 22 · 2024: 23 · 2023: 31 · 2022: 43 · 2021: 40 · 2020: 38 · 2019: 34 · 2018: 44 · 2017: 31 · 2016: 31 · 2015: 24 · 2014: 27 · 2013: 20 · 2012: 5
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Cold Spring Harbor Perspectives in Biology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (P01AG0107701, RC2AG036614)
National Institute of Neurological Disorders and Stroke (R01NS077906, R01NS040057)
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, synapses, amyloid-beta oligomers, amyloid plaques, tau tangles, presenilin, gamma-secretase, synaptic transmission, neurodegeneration, dementia
MeSH terms: Alzheimer Disease, Humans, Models, Biological, Synaptic Transmission, Synapses, Amyloid beta-Peptides, tau Proteins, Gene Transfer Techniques, Presenilins

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