ABSTRACT
Notably, a majority of patients with AD also have α-synuclein-immunoreactive Lewy bodies (LBs) in the amygdala,7,8 and a substantial proportion of them develop a form of parkinsonism: a condition denominated by
dementia with LBs.9 This suggests that factors involved in the pathogenesis of AD might promote the development of particularly aggressive forms of parkinsonism. We have recently shown that the Aβ 1-42 promotes the toxic conversion of α-synuclein and accelerates α-synuclein-dependent motor deficits.10 Moreover, it is worth taking into account the fact that both these proteins are associated with the membrane and are affected by changes in cholesterol or lipid composition.11,12 Therefore, further studies on membrane interactions and the impact of changes in the membrane during aging will help to elucidate the connection between both proteins in neurodegeneration, and efforts to gain better understanding of the relationship and the mechanisms that facilitate such pathological interactions between αsynuclein and Aβ will aid in the development of new treatment strategies for AD and PD.
