Recovery of insulin/IGF‐1/GLP‐1 signaling protects the brain against cardiometabolic and neurodegenerative diseases.

Ana Isabel Duarte

iCBR ‐ Coimbra Institute for Clinical and Biomedical Research, Faculty of Medicine, University of Coimbra, Coimbra, Coimbra, Portugal; Institute of Pharmacology and Experimental Therapeutics, Faculty of Medicine, University of Coimbra, Coimbra, Coimbra, Portugal; CIBB ‐ Center for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Coimbra, Portugal; Institute of Interdisciplinary Research (IIIUC), University of Coimbra, Coimbra, Coimbra, Portugal; CNC‐UC ‐ Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Coimbra, Portugal · pubmed

Paper

Abstract

Cardiometabolic diseases, such as type 2 diabetes, hypertension, dyslipidemia or obesity, constitute major causes of mortality and morbidity worldwide, especially among middle‐aged individuals. The increasing incidence and association with aging and lifestyle, render the cardiometabolic diseases a societal concern. This is further reinforced by their association with an increased risk of cognitive impairment and neurodegenerative diseases (namely dementia and Alzheimer’s disease (AD)). Given the poor knowledge on the precise crosslinking mechanisms between cardiometabolic and neurodegenerative diseases, we hypothesize that recovering insulin/IGF‐1/GLP‐1 signaling protects against brain and cognitive injury upon cardiometabolic diseases, ultimately preventing neurodegenerative diseases. We aimed to study the impact of recovering brain insulin/IGF‐1/GLP‐1 signaling on brain and cognitive function in animal models of cardiometabolic and neurodegenerative diseases.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper addresses the relationship between insulin/IGF-1/GLP-1 signaling and its potential protective effects against cognitive decline associated with cardiometabolic diseases, which are prevalent in aging populations. While it explores mechanisms that could contribute to longevity by potentially mitigating neurodegenerative diseases, the focus remains on treatment rather than addressing the root causes of aging itself. Thus, it represents solid research but with limited impact on the broader field of longevity.

Author of this paper? Send a correction.