Paola Giusti-Rodríguez

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Cyclin-dependent kinase 5 regulates numerous neuronal functions with its activator, p35. Under neurotoxic conditions, p35 undergoes proteolytic cleavage to liberate p25, which has been implicated in various neurodegenerative diseases. Here, we show that p25 is generated following neuronal activity under physiological conditions in a GluN2B- and(More)
Schizophrenia is strongly familial yet rarely (if ever) exhibits classical Mendelian inheritance patterns. The advent of large-scale genotyping and sequencing projects has yielded large data sets with higher statistical power in an effort to uncover new associations with schizophrenia. Here, we review the challenges in dissecting the genetics of(More)
Citation Giusti-Rodriguez, P. et al. " Synaptic Deficits Are Rescued in the p25/Cdk5 Model of Neurodegeneration by the Reduction of beta-Secretase (BACE1). Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. The MIT Faculty has made this article(More)
Alzheimer's disease (AD) is the most common cause of dementia, and is characterized by memory loss and cognitive decline, as well as amyloid β (Aβ) accumulation, and progressive neurodegeneration. Cdk5 is a proline-directed serine/threonine kinase whose activation by the p25 protein has been implicated in a number of neurodegenerative disorders. The CK-p25(More)
  • Citation Seo, Paola Jinsoo, Ying Giusti-Rodríguez, Andrii Zhou, Sukhee Rudenko, Kristie T Cho +16 others
  • 2015
The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. SUMMARY Cyclin-dependent kinase 5 regulates numerous neuronal functions with its activator, p35. Under neurotoxic conditions, p35 undergoes proteolytic cleavage to liberate p25, which has been implicated in various neurodegenerative(More)
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