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Updated: Jul 9, 2026
04:41
Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
Published on: July 14, 2010
Amyloid beta peptides and glutamatergic synaptic dysregulation
Kodeeswaran Parameshwaran1, Muralikrishnan Dhanasekaran, Vishnu Suppiramaniam
1Department of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Auburn, AL 36849, USA.
Experimental Neurology
|December 7, 2007
Summary
Alzheimer's disease involves amyloid beta peptides disrupting glutamate receptors, impairing synaptic function and causing cognitive deficits. This review explores how amyloid beta impacts these crucial brain signaling pathways.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Alzheimer's disease (AD) is characterized by amyloid beta (Abeta) peptide overproduction and accumulation.
- Abeta accumulation leads to synaptic dysfunction and cognitive deficits in early AD stages.
- Glutamate receptors are implicated in AD pathogenesis due to Abeta interactions.
Purpose of the Study:
- To review recent findings on the impact of Abeta on glutamatergic signaling in Alzheimer's disease.
- To discuss the dysregulation of synaptic glutamate receptors by Abeta.
- To highlight the link between Abeta-mediated receptor modulation and neurodegeneration.
Main Methods:
- Review of current scientific literature on Alzheimer's disease, amyloid beta, and glutamate receptors.
- Analysis of studies investigating Abeta's effects on AMPA, NMDAR, and mGluR function and expression.
- Synthesis of evidence linking glutamatergic system alterations to synaptic dysfunction and cognitive decline in AD.
Main Results:
- Abeta accumulation disrupts the function and reduces the surface expression of AMPA glutamate receptors.
- Abeta modulates N-methyl-d-aspartate receptors (NMDARs) and metabotropic glutamate receptors.
- Abeta-induced glutamate receptor modifications contribute to synaptic dysfunction and excitotoxicity.
Conclusions:
- Glutamatergic signaling is significantly compromised in Alzheimer's disease due to Abeta-induced modulation of synaptic glutamate receptors.
- These alterations in specific brain regions are critical in the progression of AD.
- Targeting Abeta-mediated glutamate receptor dysregulation may offer therapeutic strategies for AD.
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Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
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