Affiliations: Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK
Correspondence:
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Correspondence to: Nigel M. Hooper, Institute of Molecular and Cellular Biology, LIGHT Labs, Clarendon Way, University of Leeds, Leeds LS2 9JT, UK. Tel.: +44 113 343 3163; Fax: +44 113 343 5638; E-mail: n.m.hooper@leeds.ac.uk.
Abstract: The cellular form of the prion protein (PrPC) has been shown to inhibit the production of amyloid-β which is critically involved in the pathogenesis of Alzheimer's disease (AD). We examined the expression of PrPC by immunoblot analysis in the hippocampus and temporal cortex in sporadic AD, familial AD, and appropriate age-matched controls, and in an aging series (age 20 to 88 years) of brains. PrPC was reduced by 53% (p = 0.032) in the hippocampus in sporadic AD as compared to the age-matched controls. No such reduction in PrPC was seen in familial AD. PrPC was reduced in the hippocampus with aging (rs = 0.03). The reduction in PrPC in sporadic but not familial AD suggests that reduced PrPC expression reflects a primary mechanism of disease and is not merely a secondary consequence of other AD-associated changes. The reduction of PrPC in the brain with aging suggests that age-related decreases in PrPC may contribute to the increased incidence of AD in older people.
