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Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
Published on: September 3, 2014
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Synaptic protein levels altered in vascular dementia.
Lindsey I Sinclair1, Hannah M Tayler2, Seth Love2
1School of Social and Community Medicine, University of Bristol, Bristol, UK.
Neuropathology and Applied Neurobiology
|January 7, 2015
Summary
This study found reduced presynaptic proteins and increased drebrin in the temporal cortex of vascular dementia (VAD) patients, suggesting synaptic changes contribute to VAD pathogenesis.
Area of Science:
- Neuroscience
- Neuropathology
- Biochemistry
Background:
- Cerebral ischemia underlies vascular dementia (VAD), but its pathogenesis is unclear.
- Synaptic protein loss occurs in Alzheimer's disease (AD), but is understudied in VAD.
Purpose of the Study:
- To investigate synaptic protein levels in the temporal cortex of VAD patients.
- To compare synaptic protein profiles in VAD with Alzheimer's disease and non-dementia controls.
Main Methods:
- Enzyme-linked immunosorbent assays (ELISAs) measured synaptophysin, PSD-95, drebrin, SNAP-25, and VEGF in temporal cortex.
- Neuron-specific enolase corrected for neuronal content.
- Post-mortem stability of proteins was assessed.
Main Results:
- Vascular dementia (VAD) cases showed significantly lower synaptosomal-associated protein 25 (SNAP-25) levels.
- A significant increase in drebrin was observed in VAD cases.
- Synaptophysin levels were reduced in VAD compared to a second control group.
Conclusions:
- VAD likely involves a reduction in presynaptic proteins in the temporal cortex, though less pronounced than in AD.
- Increased drebrin in VAD may represent a compensatory response to diminished synaptic input.
Keywords:
DLG4 protein humanSNAP 25 protein humanapolipoproteins Edrebrinssynaptophysinvascular dementiaMore Related Videos
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