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Calcium homeostasis and development in rat hippocampal neurons, and the impact of amyloid beta proteins on neuronal function

Reference	BBS/E/B/0000L731
Principal Investigator / Supervisor	Dr Martin Bootman
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	140,601
Status	Completed
Type	Institute Project
Start date	01/10/2008
End date	30/09/2012
Duration	48 months

Abstract

Calcium is a ubiquitous messenger inside all mammalian cell types. In particular, within neurons calcium controls neurotransmitter release, communication at synapses (synapses are specialised junctions at which nerve cells communicate with other cells) and gene transcription (transfer of genetic information from DNA to RNA). Neurons employ a wide range of calcium transport mechanisms and calcium channels to generate local or global responses to stimuli. We are using a model based on cultured rat hippocampal neurons to investigate the development of neurons in culture, and the effect of amyloid beta peptide (Ab) on neuronal calcium signalling and survival. The accumulation of Ab is associated with Alzheimer's Disease (AD) in mammals, a progressive neurological disease characterised by cognitive decline resulting from selective neuronal dysfunction, synaptic loss, and neuronal cell death. It is suggested that the accumulation of extracellular plaques, consisting of aggregates of the Ab peptide, and intracellular deposits of phosphorylated Tau protein, are responsible for neuronal dysfunction and death.

Summary

unavailable

Committee	Closed Committee - Animal Sciences (AS)
Research Topics	Ageing, Neuroscience and Behaviour
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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