Gill, RS;
(2013)
The Role of Amyloid-beta in Synaptic Plasticity.
Masters thesis , University of Bristol.
Abstract
Aβ was identified in senile plaques of Alzheimer's disease brains over two decades ago and has long been regarded as a toxic by-product of APP metabolism. The "amyloid cascade hypothesis" as originally formulated is challenged by the finding that Aβ plaques do not cause cognitive decline. In this review, I highlight a growing body of evidence suggesting that Aβ plays an important physiological role as a regulator of synaptic elimination, a fundamental feature of brain plasticity. Ca2+ induced mechanisms of LTP and LTD are discussed along with the effects of Aβ on associated receptor and secondary messenger pathways. Research on Aβ and synaptic plasticity is contradictory, the effects varying with dose, cell type and disease background. The contributions of stem cell research to understanding the effects of Aβ on synaptic plasticity are also discussed and future experimental work using stem cells and the latest biophysical techniques is proposed. This dissertation summarizes the research from 26 review papers on Alzheimer's disease from PubMed over the last five years, 15 of which focused exclusively on stem cell aspects. Detailed findings are presented from 29 original research papers cited in these reviews.
| Type: | Thesis (Masters) |
|---|---|
| Title: | The Role of Amyloid-beta in Synaptic Plasticity |
| Event: | University of Bristol |
| URI: | https://discovery.ucl.ac.uk/id/eprint/1417668 |
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