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Overexpression of p25, truncated fragment of p35, Cdk5 activator causes AD like phenotypes in mice and are rescued by TFP5

Preethi Reddy Photo

Saint Louis University (Missouri)


Alzheimer’s disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually, even the ability to carry out simple tasks. Besides the hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported that cyclin-dependent kinase 5 (Cdk5), a critical neuronal kinase, is hyperactivated in AD brains and is, in part, responsible for the above pathology. Here we show that a modified truncated 24-aa peptide (TFP5), derived from the Cdk5 activator p35, after intraperitoneal (i.p.) injections, inhibits Cdk5 hyperactivity, and significantly rescues AD pathology in p25 AD model mice. The mutant mice, injected with TFP5 exhibit behavioral rescue. TFP5 does not inhibit normal Cdk5-p35 activity, and therefore has no toxic side effects. In addition, treated mice displayed rescue in spatial working memory and a reduction in phospho-neurofilaments and phospho-Tau and therefore, neurodegeneration.

Last Modified November 27, 2013