Glucagon-like peptide-1 receptor is involved in learning and neuroprotection
By M. During, Lei Cao, D. Zuzga, J. Francis, Helen L. Fitzsimons, Xiangyang Jiao, R. Bland, M. Klugmann, William A. Banks, D. J. Drucker and 1 more. Nature Medicine, 2003
849 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Endocrinology, Diabetes and Metabolism, Surgery
View Paper: https://www.semanticscholar.org/paper/61b6ac6838dc17aa68a61757dd131c0222ed18aa
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
In Endocrinology, Diabetes and Metabolism
- D. J. Drucker
- J. Meier
- M. Nauck
- Jens J. Holst
- Jonathan E. Campbell
- M. Husain
- S. Bolz
- M. H. Noyan-Ashraf
In Surgery
- D. J. Drucker
- J. Meier
- M. Nauck
- Jens J. Holst
- Jonathan E. Campbell
- M. Husain
- S. Bolz
- M. H. Noyan-Ashraf
Citations in the corpus
- An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers. (2012, neutral): “GLP1Rs are present and functional in cultured neurons as well as in rodent and human brains, and emerging evidence indicates that their stimulation regulates neuronal plasticity and cell survival (44).”
- Brain foods: the effects of nutrients on brain function (2008, neutral): “GLP1 receptors are expressed in neurons, and infusion of GLP1 into the brain has been shown to improve associative and spatial memory in rat”
- The Diabetes Drug Liraglutide Prevents Degenerative Processes in a Mouse Model of Alzheimer's Disease (2011, background): “GLP-1 analogs induce the proliferation of neuronal progenitor cells in the brains of mice (During et al., 2003).”
- Pharmacology, physiology, and mechanisms of incretin hormone action. (2013, background): “hippocampal GLP-1R expression with a recombinant adenoassociated virus ameliorated the learning deficit and decreased kainic acid-induced neurotoxicity in Glp1r / mice (During et al., 2003).”
- Intranasal delivery of biologics to the central nervous system. (2012, background): “[Ser(2)]exendin(1–9) [76] 980 Da Not determined Facilitated learning; reduced kainic-acid induced apoptosis”
- GLP-1 receptor agonists in the treatment of type 2 diabetes – state-of-the-art (2020, background): “Potential novel indications: neurodegenerative diseases and psoriasis Interest in using GLP-1 RAs to treat neurodegenerative diseases emerged from preclinical studies showing that GLP-1 receptor signaling is involved in cognitive functions [220] and GLP-1 RAs can induce neuronal growth and synaptic ”
- The physiology of glucagon-like peptide 1. (2007, background): “Thus intracerebroventricular GLP-1 administration was associated with improved learning in rats and also displayed neuroprotective effects (55, 238), and GLP-1 has been proposed as a new therapeutic agent for neurodegenerative diseases, including Alzheimer’s disease (239).”
- Glucagon-like peptide 1 (GLP-1) (2019, methodology): “In rats, central GLP-1R agonism improves several aspects of learning and memory, as demonstrated by improved performance in the Morris water maze test and by enhanced latency in the passive avoidance test [417].”
- Evaluation of intranasal delivery route of drug administration for brain targeting. (2018, neutral): “cagon/GLP-1 family) that used to facilitate learning and has been shown to decreases that IN [Ser(2)]exendin the occurence of kainic acid-induced apoptosis in mouse models after IN administration (During et al., 2003).”
- Cardioprotective and Vasodilatory Actions of Glucagon-Like Peptide 1 Receptor Are Mediated Through Both Glucagon-Like Peptide 1 Receptor–Dependent and –Independent Pathways (2008, background): “Background—The glucagon-like peptide 1 receptor (GLP-1R) is believed to mediate glucoregulatory and cardiovascular effects of the incretin hormone GLP-1(7-36) (GLP-1), which is rapidly degraded by dipeptidyl peptidase-4 (DPP-4) to GLP-1(9-36), a truncated metabolite generally thought to be inactive.”