Study sheds light on design of pharmacological strategies to treat depression in Huntington’s disease

Study sheds light on design of pharmacological strategies to treat depression in Huntington’s disease

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.

Concepts Keywords
Anxiety Nucleus accumbens
Barcelona NMDA receptor
Brain Brain-derived neurotrophic factor
Cognition PPP1R1B
Cognitive Molecular neuroscience
Cytoskeleton Addiction
Dendritic Spine Cyclin-dependent kinase 5
Depression Proteins
Dopaminergic Neurotrophic factors
Enzyme Cell cycle
Hippocampus Branches of biology
Huntington Dependent kinase dysfunction
Kinase Typical major depression
Memory Depression
Monoamine
Murine
Nervous System
Neurodegenerative
Neurogenesis
NMDA Receptor
Nucleus Accumbens
Pathology
Pharmacological
Phenotype
Phenotypes
Phosphorylation
Physiology
Physiopathology
Prefrontal Cortex
Receptors
Serotonin
Serotoninergic
Synaptic Plasticity

Semantics

Type Source Name
gene UNIPROT SMIM10L2A
gene UNIPROT SMIM10L2B
gene UNIPROT TNFSF14
disease MESH depression
gene UNIPROT CDK5
drug DRUGBANK Serotonin
gene UNIPROT PPP1R1B
pathway BSID Neurodegenerative Diseases
disease MESH Neurodegenerative Diseases
gene UNIPROT IMPACT
gene UNIPROT PTPN5
disease DOID anxiety
disease MESH anxiety
disease MESH cognitive dysfunctions

Similar

Original Article

Leave a Comment

Your email address will not be published. Required fields are marked *