Award details

The Role of Prp in Alzheimers Disease

Reference	BBS/E/A/00001665
Principal Investigator / Supervisor	Professor Jean Manson
Co-Investigators / Co-Supervisors
Institution	The Roslin Institute
Department	The Roslin Institute Department
Funding type	Research
Value (£)	55,400
Status	Completed
Type	Institute Project
Start date	01/04/2007
End date	31/03/2010
Duration	36 months

Abstract

Both the amyloid precursor protein (APP) and and PrPC are subject to proteolytic cleavage by the same zinc metalloproteases. We therefore tested the involvement of PrPC in the proteolytic processing of APP and showed the cellular production of the neurotoxic Abeta is regulated by PrPC. We now aim to examine whether this finding has implications for both Alzheimers and prion diseases. The following will be addressed: Does a decrease in PrP expression increase the progression of AD? Does A? contribute to the neurodegeneration seen in prion disease? Do A? levels alter over time in PrP knockout vs wild type mice? Do A? levels increase during the course of prion infection? Do mutations in PrP that give rise to spontaneous prion disease (e.g. P101L) increase the levels of A? in the brain.

Summary

unavailable

Committee	Closed Committee - Animal Sciences (AS)
Research Topics	Ageing, Animal Health, Neuroscience and Behaviour, TSEs (transmissible spongiform encephalopathies)
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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