Abstract
It is well documented that tauopathy is involved in various forms of neurodegenerative disease. However, there is a huge gap in terms of our understanding of the neurophysiological roles of tau, and how these can be aberrantly regulated by pathological processes. Tau is enriched in the axon but is also localized to synapses. The finding of synaptically localised tau has undoubtedly created more questions than it has answered. What is the physiological role of tau at the synapse? Whether and how does tau interact with and effect other synaptic proteins to mediate this function? Are these effects regulated by post-translational modifications of tau, such as phosphorylation? Such questions require significant attention from the scientific community if we are to resolve this critical aspect of tau biology. This chapter will describe our current understanding of synaptic tau and its functions and illuminate the numerous remaining challenges in this evolving research area.
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Abbreviations
- Aβ:
-
Amyloid beta
- AD:
-
Alzheimer’s disease
- AMPAR:
-
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor
- GSK-3:
-
Glycogen synthase kinase-3
- LTD:
-
Long-term depression
- LTP:
-
Long-term potentiation
- NMDAR:
-
N-methyl-D-aspartate receptor
- pTau:
-
Phosphorylated Tau
- Tau:
-
Microtubule associated protein tau
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Regan, P., Cho, K. (2019). The Role of Tau in the Post-synapse. In: Takashima, A., Wolozin, B., Buee, L. (eds) Tau Biology. Advances in Experimental Medicine and Biology, vol 1184. Springer, Singapore. https://doi.org/10.1007/978-981-32-9358-8_10
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