TY  - JOUR
AU  - Krüger, Lars
AU  - Mandelkow, Eva Maria
TI  - Tau neurotoxicity and rescue in animal models of human Tauopathies.
JO  - Current opinion in neurobiology
VL  - 36
SN  - 0959-4388
CY  - Philadelphia, Pa.
PB  - Current Biology
M1  - DZNE-2020-04704
SP  - 52-58
PY  - 2016
AB  - Pathological Tau is a hallmark of various neuronal disorders and spreads in the brain of Alzheimer patients in a well-defined manner. Beside Tau's main function in stabilizing microtubules for axonal transport, a variety of novel functions for neurons and glia have emerged recently. Tau regulates the susceptibility to hyperexcitation and plays a role in neuron-glia contact formation. Studies implicate soluble oligomeric species of Tau, rather than insoluble aggregates, as more detrimental to proper neuronal function. Tau is not exclusively intracellular; instead Tau can be released into the extracellular space. This has led to the hypothesis of a prion-disease like mechanism to explain the stereotypical progression of Tau. Targeting pathological Tau with antibodies or aggregation inhibitors may help to prevent pathology.
KW  - Animals
KW  - Antibodies: pharmacology
KW  - Brain: metabolism
KW  - Brain: physiopathology
KW  - Disease Models, Animal
KW  - Disease Susceptibility
KW  - Humans
KW  - Mice
KW  - Presynaptic Terminals: metabolism
KW  - Protein Aggregates: drug effects
KW  - Protein Aggregation, Pathological: metabolism
KW  - Protein Aggregation, Pathological: physiopathology
KW  - Tauopathies: metabolism
KW  - Tauopathies: physiopathology
KW  - tau Proteins: metabolism
KW  - Antibodies (NLM Chemicals)
KW  - Protein Aggregates (NLM Chemicals)
KW  - tau Proteins (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:26431808
DO  - DOI:10.1016/j.conb.2015.09.004
UR  - https://pub.dzne.de/record/138382
ER  -