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glucagon-like
285 studies tagged glucagon-like, 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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Alzheimer's disease (AD) is a devastating neurological disorder that still lacks an effective treatment, and this has stimulated an intense pursuit of disease-modifying therapeutics.
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Cognitive dysfunction and neuroinflammation are typical in Alzheimer's disease (AD), but are also associated with normal aging, albeit less severely.
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Glucagon-like peptide-1 (GLP-1) is a 30 amino acid long peptide hormone derived from the proglucagon gene and secreted in the distal small intestine when food enters the duodenum.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there is no cure.
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Type 2 diabetes mellitus (T2DM) is an important risk factor for Alzheimer's disease (AD).
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Type 2 diabetes is a risk factor for several chronic neurodegenerative disorders such as Alzheimer's or Parkinson's disease.
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Considerable overlap has been identified in the risk factors, comorbidities and putative pathophysiological mechanisms of Alzheimer disease and related dementias (ADRDs) and type 2 diabetes mellitus (T2DM), two of the most pressing epidemics of our time.
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GLP-1 signaling pathway has been well studied for its role in regulating glucose homeostasis, as well as its beneficial effects in energy and nutrient metabolism.
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38/100
Modulation of insulin-dependent signaling is emerging as a valuable therapeutic tool to target neurodegeneration.
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There are fewer than normal glucose transporters at the blood-brain barrier (BBB) in Alzheimer's disease (AD).
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Type 2 diabetes mellitus (T2DM) has been identified as a high risk factor for Alzheimer's disease (AD).
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Alzheimer's disease (AD), characterized by the aggregation of amyloid-β (Aβ) protein and neuroinflammation, is the most common neurodegenerative disease globally.
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Growing evidence suggests that agonists of glucagon-like peptide (GLP-1) receptor exert neuroprotective and neurorestorative effects across a range of experimental models of neuronal degeneration, and, recently, a pilot clinical trial of Liraglutide in Alzheimer’s disease patients showed improvements in cerebral glucose consumption that signifies disease progression.
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Although strong findings have shown the positive effects of GH/IGF-1 administration on neuroregeneration in animal models, a very limited number of clinical studies have been conducted in humans.
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Molecular communications in the gut-brain axis, between the central nervous system and the gastrointestinal tract, are critical for maintaining healthy brain function, particularly in aging.
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Type 2 diabetes mellitus (T2DM) is a complex, chronic and progressive metabolic disease, which is characterized by relative insulin deficiency, insulin resistance, and high glucose levels in blood.
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Chronic Ex-4 treatment attenuated peripheral features of T2D in GK rats, including hyperglycemia and insulin resistance.
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We here tested the hypothesis that multiple system atrophy is associated with brain insulin resistance and showed increased expression of the key downstream messenger insulin receptor substrate-1 phosphorylated at serine residue 312 in neurons and oligodendrocytes in the putamen of patients with multiple system atrophy.
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The incretins glucagon-like peptide 1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP) are growth factors that have shown neuroprotective effects in animal models of Parkinson's and Alzheimer's disease.
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Glucagon-like peptide-1 (GLP-1) is released in response to meals and exerts important roles in the maintenance of normal glucose homeostasis.
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High fat diet-induced obesity is associated with insulin resistance (IR) and other chronic, diet related illnesses, including dementia.
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Glucagon-like peptide-1 (GLP-1) is an incretin hormone shown to be active in the treatment of type-2 diabetes (T2D) and has also been shown as efficacious in Alzheimer's disease (AD).
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One of the major histopathological hallmarks of Alzheimer's disease (AD) is cerebral deposits of extracellular β-amyloid peptides.
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In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD).
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Type 2 diabetes mellitus is a risk factor for Alzheimer's disease (AD).
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Despite intensive research efforts over the past few decades, the mechanisms underlying the etiology of sporadic Alzheimer's disease (AD) remain unknown.
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Growing evidence suggests that agonists of the glucagon-like peptide 1 (GLP-1) receptor provide neuroprotection across a range of experimental models of Parkinson's disease (PD) and, recently, a small proof-of-concept, open-label human trial of exenatide in the treatment moderate severity PD appeared to show persistent improvements in motor and cognitive function.
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The evidence of strong pathological associations between type 2 diabetes and Alzheimer's disease (AD) has increased in recent years.
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36/100
Glucose-dependent insulinotropic polypeptide (GIP) is a member of the incretin hormones and growth factors.
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Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal survival and growth, serves as a neurotransmitter modulator, and participates in neuronal plasticity, which is essential for learning and memory.
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The link between diabetes mellitus and Alzheimer's disease (AD) has been known for the last few decades.
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Type 2 diabetes (T2D) is a high risk factor for Alzheimer's disease (AD).
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The incretins glucagon-like peptide 1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP) are growth factors with neuroprotective properties.
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Recent studies suggest a possible link between type 2 diabetes and Alzheimer's disease (AD).
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Increasing evidence has shown that type 2 diabetes (T2D) is a risk factor for Alzheimer's disease.
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Type 2 diabetes is a risk factor for Alzheimer's disease (AD).
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Glucagon-like peptide 1 (GLP-1) is a growth factor.
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Type 2 diabetes mellitus and Alzheimer's disease are both associated with increasing age, and each increases the risk of development of the other.
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Long-acting glucagon-like peptide-1 (GLP-1) analogues marketed for type 2 diabetes (T2D) treatment have been showing positive and protective effects in several different tissues, including pancreas, heart or even brain.
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40/100
The aim of this paper is to provide a comprehensive review of the epidemiological evidence linking type 2 diabetes mellitus and its related conditions, including obesity, hyperinsulinemia, and metabolic syndrome, to Alzheimer's disease (AD).
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Previous trials have shown promising effects of intranasally administered insulin for adults with Alzheimer's disease dementia (AD) or amnestic mild cognitive impairment (MCI).
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The emergence of glucagon-like peptide-1 as a crucial contender in modifying neurodegenerative diseases in the preclinical studies has instigated interest in investigating the antiparkinsonian effect of dipeptidyl peptidase (DPP)-4 inhibition.
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Advanced glycation end products (AGEs) consist of heterogenous group of macroprotein derivatives, which are formed by non-enzymatic reaction between reducing sugars and amino groups of proteins, lipids and nucleic acids, and whose process has progressed at an accelerated rate under diabetes.
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Recent studies indicate that glucagon-like peptide 1 (GLP-1) receptor agonists, currently used in the management of type 2 diabetes, exhibit neurotrophic and neuroprotective effects in amyloid-β (Aβ) toxicity models of Alzheimer's disease (AD).
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Type 2 diabetes is a risk factor for developing Alzheimer's disease (AD).
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Type 2 diabetes (T2D) and Alzheimer disease (AD) are two major health issues nowadays.
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Recently, it has been shown that in patients with AD (Alzheimer's disease) and, to some degree, in patients with PD (Parkinson's disease) insulin signalling is impaired.
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The incretin hormone glucagon-like peptide 1 (GLP-1) has many effects in the body.
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36/100
Insulin and Insulin Growth Factor-1 (IGF-1) play a major role in body homeostasis and glucose regulation.
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Alzheimer's disease (AD) is a progressive and degenerative disorder accompanied by cognitive impairment, but effective strategies against AD are currently not available.
From across this tag
7 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 7. The same 7 appear here every time.
- Novel GLP-1 mimetics developed to treat type 2 diabetes promote progenitor cell proliferation in the brain
- Effects of acute and chronic administration of GIP analogues on cognition, synaptic plasticity and neurogenesis in mice
- Beyond Glycemic Control: GLP-1RA–Based Therapies and Emerging Targets Beyond the Metabolic Axis
- Insulin Signaling Impairment in the Brain as a Risk Factor in Alzheimer's Disease
- Treatment with glucagon-like peptide-1 receptor agonists and incidence of dementia: Data from pooled double-blind randomized controlled trials and nationwide disease and prescription registers
- Subcutaneous administration of liraglutide ameliorates Alzheimer-associated tau hyperphosphorylation in rats with type 2 diabetes
- GLP-1 Receptor Agonists vs SGLT2 Inhibitors for Alzheimer’s Disease Risk in Type 2 Diabetes: A Systematic Review and Meta-Analysis