ReviewTherapeutic advances in neurological disorders2025
The therapeutic effects and mechanisms of glucagon-like peptide-1 receptor agonists in neurocognitive disorders.
Review in Therapeutic advances in neurological disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- GLP-1 Receptor Agonist Treatment and Health Outcomes in Methadone-Treated Patients with Opioid Use Disorder and Diabetes.Journal of general internal medicine · 2026Article
- Effects of chronic ethanol consumption on brain GLP-1R gene expression in mice and humans.Translational psychiatry · 2026Article
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
- GLP-1 Signalling as a Therapeutic Avenue in Parkinson's Disease: A Comprehensive Review.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cerebral hypoperfusion (CCH) represents a key pathogenic contributor to neurocognitive disorders. It can lead to multifaceted pathological alterations including neuroinflammation, neuronal apoptosis, blood-brain barrier disruption, synaptic plasticity deficits, and mitochondrial dysfunction. The glucagon-like peptide-1 receptor (GLP-1R), ubiquitously expressed across multiple organ systems, exerts neuroprotective effects by maintaining intracellular homeostasis and mitigating neuronal damage triggered by oxidative stress, inflammatory cascades, apoptotic signaling, and ischemic insults. Furthermore, GLP-1R activity is modulated by gut microbiota composition and short-chain fatty acid abundance, implicating the gut-brain axis in its regulatory influence on neurological function. This review systematically examines the pathophysiological mechanisms underlying CCH and highlights the therapeutic potential of GLP-1R activation. Specifically, GLP-1R-targeted interventions attenuate hypoperfusion-induced damage through pleiotropic pathways and gut-brain crosstalk, thereby offering novel perspectives for advancing both fundamental research and clinical management of neurocognitive disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.