Membrane pathology and microglial activation of mice expressing membrane anchored or membrane released forms of Aβ and mutated human Alzheimer's precursor protein (APP)
Date
2014-08-18Author
Jeffrey, Martin
McGovern, Gillian
Barron, Rona
Baumann, Frank
Metadata
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Jeffrey, M., McGovern, G., Barron, R. and Baumann, F. (2015) ‘Membrane pathology and microglial activation of mice expressing membrane anchored or membrane released forms of Aβ and mutated human Alzheimer’s precursor protein (App): Membrane pathology of anchored Aβ’, Neuropathology and Applied Neurobiology, 41(4), pp. 458–470. Available at: https://doi.org/10.1111/nan.12173.
Abstract
Alzheimer's disease and the transmissible spongiform encephalopathies or prion diseases accumulate misfolded and aggregated forms of neuronal cell membrane proteins. Distinctive membrane lesions caused by the accumulation of disease-associated prion protein (PrPd) are found in prion disease but morphological changes of membranes are not associated with Aβ in Alzheimer's disease. Membrane changes occur in all prion diseases where PrPd is attached to cell membranes by a glycosyl-phosphoinositol (GPI) anchor but are absent from transgenic mice expressing anchorless PrPd. Here we investigate whether GPI membrane attached Aβ may also cause prion-like membrane lesions.