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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
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Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?
1Menzies Research Institute, University of Tasmania, Hobart 7000, Tasmania, Australia. d.h.small@menzies.utas.edu.au
Trends in Molecular Medicine
|February 12, 2008
Summary
Alzheimer
Area of Science:
- Neuroscience
- Neurodegenerative Diseases
- Molecular Biology
Background:
- Alzheimer's disease (AD) is characterized by beta-amyloid protein (Abeta) accumulation in the brain.
- Abeta aggregation causes synaptic loss and cognitive decline.
- Mechanisms driving neurodegeneration spread in AD remain unclear.
Purpose of the Study:
- To propose synaptic scaling as a mechanism for Alzheimer's disease progression.
- To identify potential therapeutic targets for Alzheimer's disease.
Main Methods:
- Review of recent studies on synaptic plasticity in the AD brain.
- Exploration of the roles of neurotrophic factors and receptors in AD pathogenesis.
Main Results:
- Synaptic scaling, a neuronal plasticity mechanism, is hypothesized to drive AD progression.
- Brain-derived neurotrophic factor, tumor necrosis factor-alpha, and alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) are implicated in regulating synaptic scaling in AD.
Conclusions:
- Synaptic scaling may be a key factor in the spread of neurodegeneration in Alzheimer's disease.
- Further research into synaptic scaling in AD could lead to novel therapeutic strategies.
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