scispace - formally typeset
S

Sybille Krauss

Researcher at German Center for Neurodegenerative Diseases

Publications -  23
Citations -  1443

Sybille Krauss is an academic researcher from German Center for Neurodegenerative Diseases. The author has contributed to research in topics: Protein phosphatase 2 & Phosphorylation. The author has an hindex of 15, co-authored 21 publications receiving 1162 citations. Previous affiliations of Sybille Krauss include Max Planck Society & Charité.

Papers
More filters
Journal ArticleDOI

MID1, mutated in Opitz syndrome, encodes an ubiquitin ligase that targets phosphatase 2A for degradation.

TL;DR: It is shown that mutation of MID1 leads to a marked accumulation of the catalytic subunit of protein phosphatase 2A (PP2Ac), a central cellular regulator, which causes hypophosphorylation of MAPs, a pathological mechanism consistent with the OS phenotype.
Journal ArticleDOI

Inhibition of Stat3-mediated astrogliosis ameliorates pathology in an Alzheimer's disease model.

TL;DR: The data implicate Stat3‐mediated astrogliosis as an important therapeutic target in AD and suggest protective effects on network dysfunction and cognition were recapitulated in APP/PS1 mice systemically treated with a preclinical Stat3 inhibitor drug.
Journal ArticleDOI

Metformin reverses early cortical network dysfunction and behavior changes in Huntington's disease.

TL;DR: An early pattern of circuit dysregulation in the visual cortex is revealed - one of the first regions affected in premanifest Huntington’s disease - characterized by an increase in activity, an enhanced synchronicity and hyperactive neurons, and the antidiabetic drug metformin diminishes aberrant Huntingtin protein load and fully restores both early network activity patterns and behavioral aberrations.
Journal ArticleDOI

FOXO4-dependent upregulation of superoxide dismutase-2 in response to oxidative stress is impaired in spinocerebellar ataxia type 3

TL;DR: It is suggested that a decreased antioxidative capacity and increased susceptibility towards oxidative stress contributes to neuronal cell death in SCA3 and that ATXN3 plays an important role in regulating the FOXO4-dependent antioxidant stress response via SOD2.