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Cited by 235Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Amyloid beta peptides and glutamatergic synaptic dysregulation

Parameshwaran, Kodeeswaran, Dhanasekaran, Muralikrishnan, Suppiramaniam, Vishnu·2008·Experimental Neurology
DOI 10.1016/j.expneurol.2007.10.008
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Abstract

Alzheimer's disease (AD) is a major neurodegenerative disorder in which overproduction and accumulation of amyloid beta (Abeta) peptides result in synaptic dysfunction. Recent reports strongly suggest that in the initial stages of AD glutamate receptors are dysregulated by Abeta accumulation resulting in disruption of glutamatergic synaptic transmission which parallels early cognitive deficits. In the presence of Abeta, 2-amino-3-(3-hydoxy-5-methylisoxazol-4-yl) propionic acid (AMPA) glutamate receptor function is disrupted and the surface expression is reduced. Abeta has also been shown to modulate N-methyl-d-aspartate receptors (NMDARs) and metabotropic glutamate receptors. The Abeta mediated glutamate receptor modifications can lead to synaptic dysfunction resulting in excitotoxic neurodegeneration during the progression of AD. This review discusses the recent findings that glutamatergic signaling could be compromised by Abeta induced modulation of synaptic glutamate receptors in specific brain regions.

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  • Several degradation products of cellular activity, such as β-amyloid oligomers and amyloid depositions, have adverse effects on synaptic transmission and cytosolic Ca2+ concentrations and can trigger irreversible neuronal injury.

    “Several degradation products of cellular activity, such as Aβ oligomers and amyloid depositions, have adverse effects on synaptic transmission (30) and cytosolic Ca2+ concentrations (31) and can trigger irreversible neuronal injury (32).”

    From Sleep Drives Metabolite Clearance from the Adult Brain (2013) · cites this paper as [30]

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Metadata

Authors
Parameshwaran, K., Dhanasekaran, M., & Suppiramaniam, V.
Affiliations
Auburn University (US)
Corresponding author
Suppiramaniam, Vishnu
ORCID
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2008-03
Volume
210
Issue
1
Pages
7-13
ISSN
0014-4886 (ISSN-L)
DOI
10.1016/j.expneurol.2007.10.008
OpenAlex
W1980937139
Cited by
235
References
8
Citations by year
2026: 4 · 2025: 10 · 2024: 7 · 2023: 12 · 2022: 18 · 2021: 9 · 2020: 12 · 2019: 13 · 2018: 13 · 2017: 14 · 2016: 15 · 2015: 17 · 2014: 20 · 2013: 12 · 2012: 13
FWCI
0.92
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
amyloid-beta, Alzheimer's disease, glutamatergic neurotransmission, synaptic dysfunction, AMPA receptors, NMDA receptor, metabotropic glutamate receptors, excitotoxic neurodegeneration
MeSH terms
Alzheimer Disease, Animals, Humans, Models, Biological, Synaptic Transmission, Synapses, Receptors, N-Methyl-D-Aspartate, Amyloid beta-Peptides, Receptors, AMPA, Glutamic Acid

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