Retromer in Alzheimer disease, Parkinson disease and other neurological disorders.
Scott A. Small and Gregory A. Petsko
As discussed in the forum (see video here), there are many cellular pathways which are believed to be perturbed in Alzheimer’s Disease. Recent work has suggested that deficits in retromer complex function may underlie impairment of endosomal trafficking in neurons and may contribute to AD pathogenesis. This recent review illustrates the function of the retromer complex and discusses how its dysfunction may contribute to neurodegeneration.
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Nat Rev Neurosci. 2015 Mar;16(3):126-32. doi: 10.1038/nrn3896.
Also, see these selected papers for more on some of the different cellular processes which may influence AD pathogenesis:
Neurobiol Aging. 2011 Nov;32(11):2109.e1-14. doi: 10.1016/j.neurobiolaging.2011.05.025.
Altered intrinsic neuronal excitability and reduced Na+ currents in a mouse model of Alzheimer's disease.
Brown JT, Chin J, Leiser SC, Pangalos MN, Randall AD.
Trends Neurosci. 2013 Jun;36(6):325-35. doi: 10.1016/j.tins.2013.03.002.
Why size matters - balancing mitochondrial dynamics in Alzheimer's disease.
DuBoff B, Feany M, Götz J.
Neuron. 2014 Dec 3;84(5):1023-33. doi: 10.1016/j.neuron.2014.10.024.
Dendritic structural degeneration is functionally linked to cellular hyperexcitability in a mouse model of Alzheimer's disease.
Šišková Z, Justus D, Kaneko H, Friedrichs D, Henneberg N, Beutel T, Pitsch J, Schoch S, Becker A, von der Kammer H, Remy S.