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PMID: 12540051 Published · ppublish English Journal Article Review

Discovery of compounds that will prevent tau pathology.

Journal of molecular neuroscience : MN ·Vol. 19 ·No. 3 ·2002-12-00 ·Pages 261-6

Kosik KS, Ahn J, Stein R, Yeh LA

Abstract

Tau is certainly a reasonable target for the development of compounds to prevent neurofibrillary pathology, particularly in the fronto-temporal dementias. Although the mechanism of the filamentous accumulations remains unclear, sufficient knowledge is in place to move forward with high throughput screens. In fact, the development of compounds from such screens will ultimately be the only way to validate the target. The dichotomy for such screens is that in vitro screens are easier to design, but require more assumptions as to the mechanism, in contrast to cell-based screens that are more difficult to design, but make fewer assumptions about mechanism. We have designed a moderate throughput for tau binding that relies on fluorescence detection in living cells and an in vitro cdk5/p25 tau phosphorylation high throughput screen.

MeSH Terms
Animals Cyclin-Dependent Kinase 5 Cyclin-Dependent Kinases/metabolism Drug Design Drug Evaluation, Preclinical/methods Humans Mutation Nerve Tissue Proteins/metabolism Phosphorylation/drug effects Protein Binding/drug effects,physiology Tauopathies/prevention & control tau Proteins/genetics,metabolism
Chemicals
Nerve Tissue Proteins neuronal Cdk5 activator (p25-p35) tau Proteins Cyclin-Dependent Kinase 5 CDK5 protein, human Cyclin-Dependent Kinases
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Kosik Kenneth S
Harvard Medical School, Brigham and Women's Hospital, 77 Ave. Louis Pasteur, Boston, MA 02115, USA. [email protected]
Ahn Jae
Stein Ross
Yeh Li-An
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Article Info
Journal
Journal of molecular neuroscience : MN
Abbr.
J Mol Neurosci
ISSN
0895-8696
Published
2002-12-00
Pages
261-6
Language
English
Region
United States
NLM ID
9002991
Subset
IM
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