Effect of Alzheimer’s disease‐related β‐amyloid peptide conformations in transgenic mouse models of β‐amyloidosis
Résumé
Background: Alzheimer's disease (AD) brain dysfunctions are not exclusively related to amyloid plaques occurence, but are thought to start much earlier, presumably due to soluble pathological forms of b-amyloid peptide (Aβ). Indeed Aβ oligomers induce synaptic dysfunctions that cause cognitive decline, exacerbate tau pathology[1] and influence neuronal networks[2]. Although mutation-induced phenotypes are identified in AD patients, the in vivo effects of different Aβ variants are poorly understood. Here we characterized the effects of different Aβ variants in a transgenic mouse model
to provide deeper insight of transconformational processes and the subsequent alterations. Deciphering Ab profiles would help in developing new diagnostic and therapeutic approaches.
References: (1) Delacourte et al., Experimental Gerontology, 2002. (2) Bero et al., Journal of Neuroscience, 2012.
Domaines
Neurobiologie
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