Tau pathology-mediated presynaptic dysfunction

Highlights • htau42 in the presynaptic terminal induces calcium release from the ER. • The acute-modulation of IP3R and RyR by tau protein (directly or indirectly). • Identification of a synaptotoxic-tau region (PAD). • The modulation of downstream kinases by PAD.

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Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2016-06, Vol.325, p.30-38
Hauptverfasser:	Moreno, H, Morfini, G, Buitrago, L, Ujlaki, G, Choi, S, Yu, E, Moreira, J.E, Avila, J, Brady, S.T, Pant, H, Sugimori, M, Llinás, R.R
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - drug effects Animals Calcium - metabolism Cdk5 Cyclin-Dependent Kinase 5 - metabolism Decapodiformes Glycogen Synthase Kinase 3 beta - metabolism GSK3 Humans Inositol 1,4,5-Trisphosphate Receptors - metabolism IP3 receptor Neurology phosphatase-activating domain of tau Presynaptic Terminals - drug effects Presynaptic Terminals - metabolism ryanodine receptor Ryanodine Receptor Calcium Release Channel - metabolism Synaptic Transmission - drug effects tau Proteins - toxicity tauopathy
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Beschreibung
Zusammenfassung:	Highlights • htau42 in the presynaptic terminal induces calcium release from the ER. • The acute-modulation of IP3R and RyR by tau protein (directly or indirectly). • Identification of a synaptotoxic-tau region (PAD). • The modulation of downstream kinases by PAD.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2016.03.044