ePoster

Role of galectin-3 in aging and Parkinson’s disease

Ana María Espinosa Olivaand 9 co-authors
FENS Forum 2024 (2024)
Messe Wien Exhibition & Congress Center, Vienna, Austria

Presentation

Date TBA

Poster preview

Role of galectin-3 in aging and Parkinson’s disease poster preview

Event Information

Abstract

Aging is a ubiquitous biological process that results in the progressive deterioration of various organs and tissues due to the accumulation of different kind of damage throughout life. The brain is one of the most affected organs, making aging a key player in the development of neurodegenerative diseases, including Alzheimer's (AD) and Parkinson's disease (PD), the most prevalent ones.Understanding the processes occurring during aging may open up possibilities for new strategies to maintain good health throughout lifespan. Our research group has been working for years on the study of galectin-3 (Gal3), a β-galactoside-binding lectin proposed as a biomarker for metabolic disorders, cardiac fibrosis, and heart attacks. Some authors have suggested that low levels of Gal3 are associated with successful aging, as centenarians seem to have lower levels of this protein in their blood. We and others have also demonstrated a strong positive regulation of Gal3, mainly in activated microglial cells, during traumatic brain injury episodes, as well as in AD and PD, indicating a detrimental role of Gal3 in neurodegenerative diseases.In this study, we used 6 and 24-month-old wild-type (WT) and Gal3KO animals. We demonstrate for the first time that Gal3 is increased in the CNS of aged WT mice, specifically in the SN, the brain structure involved in PD. Furthermore, the results show how the absence of Gal3 in KO mice protects against many aging-related effects in various cellular phenotypes of the SN, suggesting interesting therapeutic strategies to improve brain aging and reduce the incidence of PD.

Cookies

We use essential cookies to run the site. Analytics cookies are optional and help us improve World Wide. Learn more.