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Part of the book series: Research and Perspectives in Alzheimer's Disease ((ALZHEIMER))

Abstract

Among the early changes in the brains of Alzheimer's disease patients is the loss of synapses, which is accompanied by the abnormal phosphorylation of tau protein, its missorting into the somatodendritic compartment of neurons, and its incipient aggregation. The physiological function of tau is to stabilize axonal microtubules, which enables them to carry out their role as tracks for the transport of vesicles and organelles. By implication, perturbations in the functions of tau could be related to the loss of synapses and neuronal degeneration. Cell and trans-genic animal models of tauopathy reveal that tau can indeed cause an impairment of transport in neurons. As a result, cell processes of neurons become starved, leading first to the decay of synapses and then to the loss of axons and dendrites.

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Mandelkow, EM., Thies, E., Konzack, S., Mandelkow, E. (2009). Tau and Intracellular Transport in Neurons. In: George-Hyslop, P.H.S., Mobley, W.C., Christen, Y. (eds) Intracellular Traffic and Neurodegenerative Disorders. Research and Perspectives in Alzheimer's Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-87941-1_5

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