Publication date: Jun 01, 2019
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 ScEDlvia GincE9s, VercF3nica 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.
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.
“Therefore, we considered whether alterations of Cdk5 kinase could be the main cause of depressive phenotypes in Huntington’s,” notes GincE9s, member of the Research Group of Physiopathology and Treatment of Neurodegenerative Disorders (UB-IDIBAPS).
New molecular pathways to fight depression in people with Huntington’s 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.
- Early neurochemical modifications of monoaminergic systems in the R6/1 mouse model of Huntington’s disease.