About 40% of the affected patients with Huntington’s disease -a neurodegenerative pathology- show depression symptoms, even in early stages before the apparition of the typical motor symptoms of the disease. An altered function of Cdk5 kinase -an essential enzyme in several cell signalling pathways- could explain the physiopathology of the depressive-like behaviour in Huntington’s disease, according to a pre-clinical study in which the University of Barcelona’s experts Sílvia Ginés, Verónica Brito, Albert Giralt and Jordi Alberch, from the Faculty of Medicine and Health Sciences and the Institute of Neurosciences of the UB (UBNeuro) have taken part.
The new study, published in the journal Biological Psychiatry, sheds light on the design of future pharmacological strategies -based on the modelling of specific molecular pathways- to treat depression in people with Huntington’s disease.
Cdk5 Kinase: essential protein in synaptic plasticity and memory
The study, led by the lecturer Silvia Ginés, focuses on the function of Cdk5 kinase, an essential enzyme in the neuronal function. In particular, this kinase is important in the expression, distribution and localization of the NMDA receptor family -essential in the physiology of the nervous system- and the modelling of the synaptic plasticity and learning and memory processes.
Regarding Huntington’s disease, Cdk5 kinase has a complex involvement in the apparition of cognitive dysfunctions -according to previous studies by the research team- since it is able to alter the expression and functionality of these receptors.
The role of Cdk5 in cognition is already known but there is not much known about its potential participation in depression. “Therefore, we considered whether alterations of Cdk5 kinase could be the main cause of depressive phenotypes in Huntington’s”, notes Ginés, member of the Research Group of Physiopathology and Treatment of Neurodegenerative Disorders (UB-IDIBAPS).
Read more at University of Barcelona (in Spanish)