News

Obituary

Caty Casas Louzao passed away last June 29, after a long battle with the disease.

Caty Casas was an Associate Professor in the Department of Physiology in the Department of Cell Biology, Physiology and Immunology. She was graduated in Biology in 1990, and a PhD in Cell Biology and Pathology in 2001 from the University of Barcelona. Caty Casas joined the UAB in 2004 with a reincorporation contract followed by a Juan de la Cierva contract. During the last 15 years at the UAB she has developed an intense teaching, research and management activity, generating new knowledge and contributing to the training of a new generation of doctors and researchers. Her research had focused on the study of the mechanisms involved in neurodegeneration, with particular emphasis on autophagy and endoplasmic reticulum stress, topics in which she has become an international reference. In recent years she has been the leader of the COST Transautophagy action, which brought together more than 120 European research groups. Her interest in medical application led her to patent a combination of drugs with proven protective and regenerative effect for nerve injuries, NeuroHeal, and to found a technology-based company for its potential clinical use.

Their colleagues from the Neuroplasticity and Regeneration research group, the Medical Physiology Unit, the Department and the Institute of Neurosciences come together to express their deep condolences

NEUROGRAPH project

 

 

A graphene EcoG Microtransistorsfabricated by ICN2 and CNM groups of the graphcat consortium similar to the ones that will be used in the Neurograph project, . Image credit: Nature Materials, media.springernature.com

 

The Direcció General de Recerca de la Generalitat de Catalunya resolved, on December 19th 2019, to provide co-funding from the FEDER funds to the emerging technologies consortium GRAPHCAT.

Within GRAPHCAT, the Group NPiR in cooperation with the Group of Vascular Pharmacology of the UAB, takes part in the subproject NEUROGRAPH: Monitoring Cortical Depolarization in Neurointensive Care using Graphene EcoG Microtransistors.

The UAB team will explore models of brain lesion by ischemia and attempt to validate the application of CSD detection for predicting spreading of brain damage. In addition, novel therapeutic agents will be investigated in order to construct a close-loop system of detection-treatment to reduce the extension of the ischemic brain area.

The UAB Neurograph team is leaded by Drs. Jaume del Valle, Francesc Jiménez and Xavier Navarro.

Gene therapy for overexpressing Neuregulin 1 promotes functional improvement in the SOD1 ALS mice

In two recently published papers, members of the Group NP&R showed that overexpression of Neuregulin 1, mediated by gene therapy, improved the evolution of the disease in the SOD1G93A mouse model of Amyotrophic Lateral Sclerosis (ALS). They suggest that this therapy could be considered in the future as a treatment for ALS.

In the first, an AAV vector was injected intravascularly to increase NRG1-type I in the mouse muscles. The results showed that SOD1G93A mice with higher levels of NRG1-I began to develop symptoms of the disease later, and had a slower disease progression than the controls. In addition, this therapy promoted an increase of the number of surviving motoneurons in the spinal cord compared to control mice, as well as improved preservation of their connections with skeletal muscles.

Mòdol-Caballero G, et al. Gene therapy for overexpressing Neuregulin 1 type I in skeletal muscles promotes functional improvement in the SOD1(G93A) ALS mice. Neurobiol Dis 2020; 137:104793. doi: 10.1016/j.nbd.2020.104793.

In the second paper, we used gene therapy based on intrathecal administration of AAV virus to overexpress NRG1-III in the spinal cord of SOD1G93A mice. Our results indicate that overexpression of NRG1-III preserved neuromuscular function of the hindlimbs, improved locomotor performance, increased the number of surviving MNs, and reduced glial reactivity in the treated female SOD1G93A mice. However, NRG1-III did not have a significant effect on male mice, indicating relevant sex differences.

Mòdol-Caballero G, et al. Therapeutic role of Neuregulin 1 Type III in SOD1-linked Amyotrophic Lateral Sclerosis. Neurotherapeutics 2020 in press. doi: 10.1007/s13311-019-00811-7.

Project funded to develop a new treatment to stop ALS

The project lead by Rubén López-Vales, from the Group NPiR, entitled "A new treatment to stop the progression of amyotrophic lateral sclerosis (ALS)", will investigate the contribution of a new family of lipids to modulate neuroinflammation in mice with ALS, looking for a new therapy that will be more effective than the current ones. The objective is to stop the progression of ALS and find new biomarkers that predict their evolution.

The project has been selected, after a rigorous selection process with the participation of more than 250 experts, and will receive a maximum of 500,000 euros, which will be provided by the "La Caixa" Foundation and the Luzón Foundation.

Group of Neuroplasticity and Regeneration

The research activities of the Group focus on the study of physiopathological mechanisms of neural lesions, neuropathic pain and neurodegeneration, and on the application of novel therapeutic strategies for regenerating traumatic and degenerative lesions of the nervous system.

The members of the group have combined expertise in microsurgery, neurophysiology, rehabilitation, morphology, cell culture, cellular and molecular neurobiology, bioelectronics and immunology.

The group has established cooperative research in clinical neurosciences, particularly on new nerve repair therapies with the Hospital Clinic of Barcelona, in modulation of neural plasticity after brain and spinal cord lesions with the Institute Guttmann of Neurorehabilitation, and in motoneuron diseases and neuropathies with the Hospital of Bellvitge.

Which are the research lines of the group?

What can the group offer?