Publication date: Jun 01, 2019
An altered function of Cdk5 kinase -an essential enzyme in several cell signaling pathways- could explain the physiopathology of the depressive-like behavior in Huntington’s disease, according to a pre-clinical study in which the UB experts ScEDlvia GincE9s, VercF3nica Brito, Albert Giralt and Jordi Alberch, from the Faculty of Medicine and Health Sciences and the Institute of Neurosciences of the University of Barcelona (UBNeuro) have taken part.
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 results of this study showed that in murine models with the disease, Cdk5 shows a higher activity in two brain regions -the nucleus accumbens and the prefrontal cortex- that are associated with anxiety and depression processes.
“It would be necessary to avoid unwanted effects in other physiological pathways where this enzyme is active, and this would require defining which molecules the Cdk5 kinase acts on -in a non-functional manner to create the depressive-like phenotype”, comments lecturer ScEDlvia GincE9s.
Finding out whether the alteration in Cdk5 kinase affects one of the neuronal sub-populations -with contraposed effects in depression- integrating the nucleus accumbens, the main brain region affected by the Cdk5 altered function, will be another challenge for the research team.
- Early neurochemical modifications of monoaminergic systems in the R6/1 mouse model of Huntington’s disease.
- Reduced nucleus accumbens enkephalins underlie vulnerability to social defeat stress.