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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Bibliographic Details
Published inNeuroscience Vol. 325; pp. 30 - 38
Main Authors 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 Journal Article
LanguageEnglish
Published United States Elsevier Ltd 14.06.2016
Subjects
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
tauopathy
cyclin-dependent protein kinase 5
frontotemporal dementia
ER
IP3 receptor
PAD
phosphatase-activating domain of tau
Cdk5
GSK3
FTD
FAT
fast axonal transport
ryanodine receptor
endoplasmic reticulum
glycogen synthase kinase 3
phosphatase-activating domain
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Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2016.03.044