Cellular Mechanisms of Alzheimer's Disease: by C. Haass, G. Multhaup

By C. Haass, G. Multhaup

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Extra info for Cellular Mechanisms of Alzheimer's Disease: Neurodegenerative Diseases 2006

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These results suggest that disruption of axoNeurodegenerative Dis 2006;3:218–226 223 nal transport and synaptic transmission may be key components of the pathogenic mechanism that underlie neuronal dysfunction in the early stages of tauopathies. It will be interesting whether changes in the dose of APP/ APPL, which also affect the axonal transport of synaptic vesicles and morphology of synapses in mouse and Drosophila models, may also lead to altered synaptic plasticity, thought to represent the neurophysiological correlate of learning and memory [82, 83].

One of them, spe-4, is only expressed in spermatids during spermatogenesis. Its function involves the correct transport and formation of intracellular organelles and will be described in detail elsewhere. The two other C. elegans presenilin genes, sel-12 (suppressor/enhancer of lin-12) and hop-1 (homolog of presenilin) have similar functions and can substitute for one another. hop-1;sel-12 double mutants completely inhibit signaling through the two C. elegans Notch receptors glp-1 and lin-12, underscoring their fundamental role for Notch signaling.

A The diagram summarizes known or plausible modes of MARK regulation which would affect the phosphorylation of tau and hence the stability of microtubules and the aggregation of tau. (a) Activation via phosphorylation by MARKK at the activation loop (T208) [29]. (b) Inhibition by binding of PAK5 to the catalytic domain [31]. (c) Regulation by interaction of the UBA domain with ubiquitin (not proven, but suggested by X-ray structure) [7]. (d) Regulation by interaction of the CD motif with a cofactor, in analogy with MAP kinases where upstream or downstream kinases can be bound [7, 54].

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