The cellular phase of Alzheimer’s Disease: from genes to cells
Bart De Strooper · UK Dementia Research Institute, UCL, London & & KU Leuven & VIB Center for Brain and Disease Research, Belgium KU Leuven & VIB Center for Brain and Disease Research, Belgium
Thu, Oct 1, 2020 · 12:15 UTC
The amyloid cascade hypothesis for Alzheimer disease ((Hardy and Selkoe, 2002; Hardy and Higgins, 1992; Selkoe, 1991), updated in (Karran et al., 2011) provides a linear model for the pathogenesis of AD with Aβ accumulation upstream and Tau pathology, inflammation, synaptic dysfunction, neuronal loss and dementia downstream, all interlinked, initiated and driven by Aβ42 peptides or oligomers. The genetic mutations causing familial Alzheimer disease seem to support this model. The nagging problem remains however that the postulated causal, and especially the ’driving’ role of abnormal Aβ aggr