ArticleBrain research2009
Disruption of glutamate receptors at Shank-postsynaptic platform in Alzheimer's disease.
Article in Brain research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- The glutamatergic system in Alzheimer's disease: a systematic review with meta-analysis.Molecular psychiatry · 2024Pooled it
- Continuous monitoring of glutamate using electroactive templated polymers as synthetic molecular receptors.The Analyst · 2026Article
- ZCCHC17: a target for synaptic dysfunction and neuronal excitability in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Demyelination-induced glutamatergic imbalance mediates hippocampal Hyperexcitability.Neurobiology of disease · 2025Article
- ZCCHC17 knockdown phenocopies Alzheimer's disease-related loss of synaptic proteins and hyperexcitability.Journal of neuropathology and experimental neurology · 2024Article
- Factor H's Control of Complement Activation Emerges as a Significant and Promising Therapeutic Target for Alzheimer's Disease Treatment.International journal of molecular sciences · 2024Article
- Postsynaptic Protein Shank3a Deficiency Synergizes with Alzheimer's Disease Neuropathology to Impair Cognitive Performance in the 3xTg-AD Murine Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- Association of SHANK Family with Neuropsychiatric Disorders: An Update on Genetic and Animal Model Discoveries.Cellular and molecular neurobiology · 2022Review
- The Peptidyl-prolyl Isomerase Pin1 in Neuronal Signaling: from Neurodevelopment to Neurodegeneration.Molecular neurobiology · 2021Review
- Preservation of dendritic spine morphology and postsynaptic signaling markers after treatment with solid lipid curcumin particles in the 5xFAD mouse model of Alzheimer's amyloidosis.Alzheimer's research & therapy · 2021Article
- SHANK2 mutations impair apoptosis, proliferation and neurite outgrowth during early neuronal differentiation in SH-SY5Y cells.Scientific reports · 2021Article
- Impaired Learning and Memory Ability Induced by a Bilaterally Hippocampal Injection of Streptozotocin in Mice: Involved With the Adaptive Changes of Synaptic Plasticity.Frontiers in aging neuroscience · 2021Article
- Neuroproteomics of the Synapse: Subcellular Quantification of Protein Networks and Signaling Dynamics.Molecular & cellular proteomics : MCP · 2021Review
- TDP-43 proteinopathy impairs mRNP granule mediated postsynaptic translation and mRNA metabolism.Theranostics · 2021Article
- Acetylation of AMPA Receptors Regulates Receptor Trafficking and Rescues Memory Deficits in Alzheimer's Disease.iScience · 2020Article
- Bayesian integrative analysis of epigenomic and transcriptomic data identifies Alzheimer's disease candidate genes and networks.PLoS computational biology · 2020Article
- A NeurotoxicFrontiers in molecular neuroscience · 2020Review
- Amyloid Beta Oligomers Target to Extracellular and Intracellular Neuronal Synaptic Proteins in Alzheimer's Disease.Frontiers in neurology · 2019Article
- Effect of intraperitoneal or intracerebroventricular injection of streptozotocin on learning and memory in mice.Experimental and therapeutic medicine · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic loss underlies the memory deficit of Alzheimer's disease (AD). The molecular mechanism is elusive; however, excitatory synapses organized by the postsynaptic density (PSD) have been used as targets for AD treatment. To identify pathological entities at the synapse in AD, synaptic proteins were screened by quantitative proteomic profiling. The critical proteins were then selected for immunoblot analysis. The glutamate receptors N-methyl-d-aspartate (NMDA) receptor 1 and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor 2 (GluR2) were substantially lost; specifically, the loss of GluR2 was up to 40% at PSD in AD. Shank proteins, the organizers of these glutamate receptors at excitatory synapses, were dramatically altered in AD. The level of Shank2 was increased, whereas the protein level of Shank3 was decreased. Further, the Shank3 protein was modified by ubiquitin, indicating that abnormal activity of the ubiquitin-proteasome system may lead to Shank3 degradation in AD. Our findings suggest that disruption of glutamate receptors at the Shank-postsynaptic platform could contribute to destruction of the PSD which underlies the synaptic dysfunction and loss in AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.