Dendritic Spine Loss and Synaptic Alterations in Alzheimer’s Disease
Open accessAbstract
Dendritic spines are tiny protrusions along dendrites, which constitute major postsynaptic sites for excitatory synaptic transmission. These spines are highly motile and can undergo remodeling even in the adult nervous system. Spine remodeling and the formation of new synapses are activity-dependent processes that provide a basis for memory formation. A loss or alteration of these structures has been described in patients with neurodegenerative disorders such as Alzheimer's disease (AD), and in mouse models for these disorders. Such alteration is thought to be responsible for cognitive deficits long before or even in the absence of neuronal loss, but the underlying mechanisms are poorly understood. This review will describe recent findings and discoveries on the loss or alteration of dendritic spines induced by the amyloid beta (Abeta) peptide in the context of AD.
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Dystrophic neurites are associated with amyloid plaques in Alzheimer's disease brains.
“Dystrophic neurites are also associated with amyloid plaques in the brains of individuals with Alzheimer’s disease19,20.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [20]
Drebrin is reduced in the brains of individuals with Alzheimer's disease and in transgenic animal models.
“Drebrin, a postsynaptic protein that binds and stabilizes actin in spines, is reduced in the brains of individuals with Alzheimer’s disease and in transgenic animal models of the disease20.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [20]
Active cofilin causes actin destabilization, and much evidence supports a role for cofilin in neurodegeneration, including Alzheimer's disease.
“Active cofilin causes actin destabilization and much evidence supports a role for cofilin in neurodegeneration, including Alzheimer’s disease20.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [20]
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References 120 · Cited by 296
- Authors
- Knobloch, M., & Mansuy, I. M.
- Affiliations
- University of Zurich (CH)
- Corresponding author
- Mansuy, Isabelle M.
- Venue
- Molecular Neurobiology
- Published
- 2008-02
- Volume
- 37
- Issue
- 1
- Pages
- 73-82
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W2058371877
- Cited by
- 296
- References
- 120
- Citations by year
- 2026: 13 · 2025: 11 · 2024: 8 · 2023: 21 · 2022: 12 · 2021: 9 · 2020: 15 · 2019: 11 · 2018: 12 · 2017: 9 · 2016: 17 · 2015: 13 · 2014: 19 · 2013: 32 · 2012: 25
- FWCI
- 15.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- reroDoc Digital Library (submittedVersion)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- ETH Zürich Research Collection
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- dendritic spines, Alzheimer's disease, amyloid-beta, synaptic loss, postsynaptic sites, excitatory synapses, cognitive impairment, neurodegeneration, memory formation
- MeSH terms
- Alzheimer Disease, Animals, Cerebral Cortex, Cognition Disorders, Cytoskeleton, Humans, Nerve Degeneration, Synaptic Transmission, Synapses, Amyloid beta-Peptides, Dendritic Spines
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