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glp-1
285 studies tagged glp-1, dated 1994-05-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- The metabolic-brain axis: GLP-1 signaling, insulin resistance, and obesity pharmacotherapy in neurodegeneration 2026-10-30
- Beyond Glycemic Control: The Pleiotropic Role of GLP-1RAs and Melatonin in Combating Neuroinflammation and Mitochondrial Dysfunction 2026-10-28
- PFKFB3 inhibition restores β-cell responsiveness to acetylcholine in a 3xTg-AD pancreatic tissue-slice model 2026-10-07
Studies
285 studies carry this tag.
Date range
1994 to 2026
Top journals
- International journal of molecular sciences 10
- Neuropharmacology 10
- Journal of Alzheimer's disease : JAD 9
- European journal of pharmacology 8
- Neurobiology of aging 6
177 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Type 2 (T2) diabetes mellitus (DM) has been associated with an increased incidence of neurodegenerative disorders, including Alzheimer's disease (AD).
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Type 2 diabetes has been identified as a risk factor for Alzheimer's disease (AD).
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Type 2 diabetes has been identified as a risk factor for patients with Alzheimer's disease.
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We tested here the impact of a long-term inhibition of dipeptidyl peptidase-4 (DPP-4) with sitagliptin on the deposition of amyloid-beta within the brain and deficits in memory-related behavioral paradigms in a model of Alzheimer's disease (AD): double transgenic mice B6*Cg-Tg(APPswe,PSEN1dE9)85Dbo/J. Mice began to receive sitagliptin at 7 months of age.
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Both insulin resistance (type II diabetes) and beta-amyloid (Abeta) oligomers are implicated in Alzheimer's disease (AD).
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Type 2 diabetes has been identified as a risk factor for Alzheimer disease (AD).
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Patients with long-standing diabetes commonly develop diabetic encephalopathy, which is characterized by cognitive impairment and dementia.
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There is a cluster of risk factors for Type 2 diabetes and vascular disease that include high blood glucose, obesity, high blood pressure, increased blood triacylglycerols and insulin resistance.
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Epidemiological, clinical and experimental evidence suggests a link between type 2 diabetes and Alzheimer's disease (AD).
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Synapse deterioration underlying severe memory loss in early Alzheimer's disease (AD) is thought to be caused by soluble amyloid beta (Abeta) oligomers.
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Type 2 diabetes has been identified as a risk factor for Alzheimer's disease (AD).
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Accumulation and deposition of amyloid beta peptide (Abeta) in the brain causes neuronal apoptosis and eventually leads to Alzheimer's disease (AD).
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Intranasal insulin administration raises central nervous system (CNS) insulin levels in humans and acutely facilitates verbal memory in patients with Alzheimer's disease (AD), an effect that may differ by APOE genotype.
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36/100
Type 2 diabetes mellitus has been identified as a risk factor for Alzheimer's disease, and insulin signalling is often impaired in Alzheimer's disease, contributing to the neurodegenerative process.
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Recent studies have indicated an association between Alzheimer's disease (AD) and central nervous system (CNS) insulin resistance.
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Alzheimer's disease (AD) is the most common form of dementia.
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36/100
The cascade of Alzheimer's disease (AD) neurodegeneration is associated with persistent oxidative stress, mitochondrial dysfunction, impaired energy metabolism, and activation of pro-death signaling pathways.
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A number of well-designed epidemiological studies have linked type 2 diabetes mellitus (T2DM) with an increased risk of Alzheimer's disease (AD).
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Reduced glucose utilization and energy metabolism occur early in the course of Alzheimer's disease (AD) and correlate with impaired cognition.
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Glucagon-like peptide-1 (7-36)--amide (GLP-1) is an endogenous insulinotropic peptide that is secreted from the gastrointestinal tract in response to food.
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Raising insulin acutely in the periphery and in brain improves verbal memory.
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The neurodegeneration that occurs in sporadic Alzheimer's disease (AD) is consistently associated with a number of characteristic histopathological, molecular, and biochemical abnormalities, including cell loss, abundant neurofibrillary tangles and dystrophic neurites, amyloid-beta deposits, increased activation of pro-death genes and signaling pathways, impaired energy metabolism/mitochondrial function, and evidence of chronic oxidative stress.
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G protein-coupled receptors (GPCRs) play pivotal roles in regulating the function and plasticity of neuronal circuits in the nervous system.
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Previous studies have suggested an acutely improving effect of insulin on memory function.
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Three closely related forms of glycogen synthase kinase 3 (GSK-3alpha, GSK-3beta and GSK-3beta2) have a major role in Wnt and Hedgehog signaling pathways and regulate the cell-division cycle, stem-cell renewal and differentiation, apoptosis, circadian rhythm, transcription and insulin action.
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Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an endogenous 30-amino acid gut peptide, which binds at the GLP-1 receptor coupled to the cyclic AMP second messenger pathway.
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Recent epidemiological evidence indicates that insulin resistance, a proximal cause of Type II diabetes [a non-insulin dependent form of diabetes mellitus (NIDDM)], is associated with an increased relative risk for Alzheimer's disease (AD).
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In recent years, VIP/PACAP/secretin family has special interest.
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Glucagon-like peptide-1(7-36)-amide (GLP-1) is an endogenous insulinotropic peptide that is secreted from the gastrointestinal tract in response to food.
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Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an insulinotropic hormone, secreted from the enteroendocrine L cells of the intestinal tract in response to nutrient ingestion.
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36/100
Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an endogenous insulinotropic peptide that is secreted from the L cells of the gastrointestinal tract in response to food.
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The insulinotropic hormone glucagon-like peptide-1 (7-36)-amide (GLP-1) has potent effects on glucose-dependent insulin secretion, insulin gene expression, and pancreatic islet cell formation and is presently in clinical trials as a therapy for type 2 diabetes mellitus.
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Glycogen synthase kinase 3 (GSK-3) is a serine/threonine protein kinase that has recently emerged as a key target in drug discovery.
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Extensive evidence indicates that relatively modest increases in circulating glucose concentrations enhance learning and memory processes in rodents and humans.
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Glucose metabolism is depressed in the temporal and parietal regions of the cortex in patients with Alzheimer's disease.
From across this tag
9 of the 285 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Effects of GLP-1 receptor agonists on neurological complications of diabetes
- GLP-1 Receptor Agonists in Neurodegeneration: Neurovascular Unit in the Spotlight
- Neurodegeneration onset with glucagon-like peptide-1 receptor agonists in people with type 2 diabetes: a real-world multinational cohort study
- Mechanistic insight into the role of metformin in Alzheimer's disease
- The potential role of human islet amyloid polypeptide in type 2 diabetes mellitus and Alzheimer's diseases
- Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis
- Insulin resistance and exendin-4 treatment for multiple system atrophy
- Diabetes and Alzheimer's disease crosstalk
- In Alzheimer's Disease, 6-Month Treatment with GLP-1 Analog Prevents Decline of Brain Glucose Metabolism: Randomized, Placebo-Controlled, Double-Blind Clinical Trial