Parkinson's disease and brain insulin signaling: Mechanisms and potential role of GLP-1 mimetics

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dc.authorid0000-0003-4056-1673
dc.contributor.authorForoozanmehr, Behina
dc.contributor.authorHemmati, Mohammad Amin
dc.contributor.authorYaribeygi, Habib
dc.contributor.authorKarav, Sercan
dc.contributor.authorJamialahmadi, Tannaz
dc.contributor.authorSahebkar, Amirhossein
dc.date.accessioned2026-02-03T12:02:47Z
dc.date.available2026-02-03T12:02:47Z
dc.date.issued2025
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractParkinson's disease (PD) is a common neurodegenerative disorder characterized primarily by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. The pathophysiology of PD is complex and multifactorial involving genetic factors, oxidative stress, mitochondrial dysfunction, impaired protein clearance, and neuroinflammation but recent evidence emphasizes the role of impaired brain insulin signaling. Insulin is a metabolic hormone with extensive effects on metabolic substrates but recent studies have demonstrated that it is also involved in central signaling pathways and induces different brain areas related to food craving, motor activities, cognitive abilities, and emotional feelings. Hence, it has been suggested that induction of brain insulin sensitivity may be a promising treatment for PD. Glucagon-like peptide-1 (GLP-1) mimetics are a new-generation class of antidiabetics that normalize glucose homeostasis via several pathways. Recent studies suggest extraglycemic benefits for GLP-1 mimetics against PD. GLP-1 mimetics can prevent or slow PD progression. Additionally, these agents can improve cognitive functions by improving brain insulin signaling pathways. In this review, we aim to highlight the role of brain insulin signaling in PD pathophysiology and discuss the possible benefits of GLP-1 mimetics in PD management.
dc.identifier.doi10.1016/j.brainres.2025.149738
dc.identifier.issn0006-8993
dc.identifier.issn1872-6240
dc.identifier.pmid40449678
dc.identifier.scopus2-s2.0-105006877186
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.brainres.2025.149738
dc.identifier.urihttps://hdl.handle.net/20.500.12428/34871
dc.identifier.volume1862
dc.identifier.wosWOS:001503682900001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofBrain Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20260130
dc.subjectDiabetes mellitus
dc.subjectParkinson's disease
dc.subjectBrain insulin signaling
dc.subjectGLP-1 mimetics
dc.titleParkinson's disease and brain insulin signaling: Mechanisms and potential role of GLP-1 mimetics
dc.typeArticle

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