PubMed: 30640040

Screening of a neuronal cell model of tau pathology for therapeutic compounds.
Neurobiology of aging
Denner P | Fava E | Kitanovic A | Kurkowsky B | Mandelkow E | Möhl C | Pickhardt M | Tassoni M

Evidence 88b3036d50

As shown before, Tau aggregation (on the level of oligomeric and/or fibril aggregates) is toxic for cells.

Evidence b4cb85983f

Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control.

Evidence f011744b02

Treatment with Givinostat (1.2 µM) lead to a nearly 7-fold increase in the fraction of ThS + cells (from ~ 12% to ~ 84%, Fig. S4A and B, blue lines) compared to the uninduced control, and 2.5-fold compared to the induced control.

Evidence d00eb97691

Conversely, compounds related to HDAC inhibition (16 of 20) led to enhanced Tau aggregation, suggesting that HDAC activity is important for suppressing aggregation

Evidence b8b0708f78

The dose response screening identified compounds related to the inhibition of 3 major targets led to inhibition of Tau aggregation: p38 MAPK (7 out of 8 compounds in the initial library), VEGFR1/2 (3 of 8) and TGF (3 of 10).


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