Journal
NEURON
Volume 99, Issue 1, Pages 13-27Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2018.06.003
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Funding
- National Health and Medical Research Council [1081916, 1132524, 1136241, 1143848, 1143978]
- Australian Research Council [DP170100781, DP170100843]
- CurePSP [609-2015-07]
- National Health and Medical Research Council of Australia [1081916, 1143978, 1136241, 1143848] Funding Source: NHMRC
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The microtubule-associated protein tau and amyloid-beta (A beta) are key players in Alzheimer's disease (AD). A beta and tau are linked in a molecular pathway at the post-synapse with tau-dependent synaptic dysfunction being a major pathomechanism in AD. Recent work on site-specific modification of dendritic and more specifically post-synaptic tau has revealed new endogenous functions of tau that limits synaptic A beta toxicity. Thus, molecular studies opened a newperspective on tau, placing it at the center of neurotoxic and neuroprotective signaling at the post-synapse. Here, we review recent advances on tau in the dendritic compartments, with implications for understanding and treatment of AD and related neurological conditions.
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