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peptide-1
285 studies tagged peptide-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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Alzheimer's disease (AD) is a progressive neurodegenerative disease, also regarded as "type 3 diabetes" for the last few years because of the brain insulin resistance (IR) and dysregulation of insulin signaling in the brain, which can further promote pathological progression of AD.
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We revealed GLP-1's capacity to regulate astrocytic glycolysis, providing mechanistic insight into one of its neuroprotective roles in AD and support for the feasibility of energy regulation treatments for AD.
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Recent clinical and epidemiological studies support the contention that diabetes mellitus (DM) is a strong risk factor for the development of Alzheimer's disease (AD).
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40/100
Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of antidiabetic drugs that improve the glycaemia via several molecular pathways.
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Our results provide a clue for the hypothesis that autophagy enhancement and apoptosis inhibition may be involved in the effect of semaglutide to protect against Aβ 25-35 .
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Among the more promising treatments proposed for Alzheimer's disease (AD) and Parkinson's disease (PD) are those reducing brain insulin resistance.
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Insulin is a peptide secreted by the pancreas and plays an important role in the regulation of glucose metabolism in peripheral tissues.
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Different concentrations of OA were able to induce apoptosis of SH-SY5Y cells in a dose-dependent manner.
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Metabolic syndrome (MetS) is an association between obesity, dyslipidemia, hyperglycemia, hypertension, and insulin resistance.
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Emerging evidence suggest that dimethylbiguanide (metformin), a first-line drug for type 2 diabetes mellitus, could be neuroprotective in a range of brain pathologies, which include neurodegenerative diseases and brain injury.
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The discovery that glucagon-like peptide 1 (GLP-1) mediates a significant proportion of the incretin effect during the postprandial period and the subsequent observation that GLP-1 bioactivity is retained in type 2 diabetes (T2D) led to new therapeutic strategies being developed for T2D treatment based on GLP-1 action.
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This review evaluates the novel strategy of treating Alzheimer's and Parkinson's disease (AD and PD) withdrugs that initially have been developed to treat type 2 diabetes.
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Alzheimer's disease (AD) is the most common form of dementia worldwide, being characterized by the deposition of senile plaques, neurofibrillary tangles (enriched in the amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau), respectively) and memory loss.
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Neuronal insulin resistance is a significant feature of Alzheimer's disease (AD).
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Patients with diabetes and epilepsy are more prone to cognitive impairment, dementia, and even Alzheimer's disease.
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Liraglutide might slow down memory function decline in diabetic patients in early, and possibly preclinical stages of the disease.
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Our results demonstrate that DA5‐CH has neuroprotective effects in the STZ‐induced animal model and that DA5‐CH has potential to treat neurodegenerative disorders such as AD.
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Alzheimer disease (AD) may develop after the onset of type 2 diabetes mellitus (T2DM), and the risk of AD may depend on the antidiabetic drug administered.
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Alzheimer's disease (AD) is a neurodegenerative disorder for which there is no cure.
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Vildagliptin (Vilda), a dipeptidyl peptidase-4 (DPP-4) inhibitor, has been highlighted as a promising therapeutic agent for neurodegenerative diseases as Alzheimer's and Parkinson's diseases.
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Glucose-dependent Insulinotropic polypeptide (GIP) is a peptide hormone of the incretin family.
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Alzheimer's disease (AD) is the most prevalent form of dementia, particularly in old age subjects.
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Concomitant diseases in elderly individuals with diabetes (renal failure, heart failure, ischemic heart disease, stroke, urinary incontinence, cognitive impairment, dementia, sarcopenia, and osteoporosis) make diabetes management difficult.
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These data suggest that the neuroprotective effects of liraglutide on diabetes-induced cognitive impairments are associated with the improvements of hippocampal synapses and inhibition of neuronal apoptosis.
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Glucagon-like peptide-1 (GLP-1) signaling in the brain plays an important role in the regulation of glucose metabolism, which is impaired in Alzheimer's disease (AD).
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Insulin resistance is a major risk factor for Alzheimer's disease (AD).
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Currently there is no effective therapy available for cognitive impairments in Down syndrome (DS), one of the most prevalent forms of intellectual disability in humans associated with the chromosomes 21 trisomy.
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The role of mitochondrial dysfunction has been well-documented in Alzheimer's disease (AD).
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One hundred and fifty years ago, Paul Langerhans described what would come to be known as pancreatic 'islet of Langerhans'.
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Type 2 diabetes is a risk factor for developing Alzheimer's disease (AD).
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Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells.
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Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer's disease, Parkinson's disease or vascular occlusion.
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The current absence of effective treatments for Alzheimer's disease (AD) and Parkinson's disease (PD) reflects an incomplete knowledge of the underlying disease processes.
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Liraglutide is a GLP-1 analog (glucagon like peptide-1) used primarily in the treatment of diabetes mellitus type 2 (DM2) and obesity.
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Dulaglutide, a novel long-acting glucagon-like peptide 1 (GLP-1) receptor agonist, is an incretin mimetic approved for type 2 diabetes mellitus (T2DM) treatment.
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In MCI/AD, both the CSF and serum samples had significantly elevated mean levels of C-peptide and an incretin, and reduced expression of Visfatin, whereas only CSF showed significant reductions in insulin and leptin and only serum had increased glucagon, PAI-1, and ghrelin.
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Single-cell digital PCR revealed GLP-1 receptor expression in neurogliaform cells and showed that copy numbers of mRNA of the Glp1r gene in hyperglycaemia exceeded those in hypoglycaemia by 9.6 times (p < 0.008).
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Hyperhomocysteinemia (Hhcy) is an independent risk factor for Alzheimer's disease (AD), and insulin-resistance is commonly seen in patients with Hhcy.
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The positive finding of lower EV Aβ42 supports emerging evidence that plasma neuronal EVs provide an effective platform for demonstrating biomarker responses in clinical trials in AD.
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Geniposide, an iridoid glycoside extract from the gardenia fruit, is used in traditional Chinese medicine to alleviate symptoms of liver and inflammatory diseases.
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Incretin contains two peptides named glucagon-like peptide-1(GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).
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39/100
Neurodegenerative disorders are the most devastating disorder of the nervous system.
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Recently, Alzheimer's disease (AD) is understood as "diabetes of the brain" or "type 3 diabetes."
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Obesity and type 2 diabetes mellitus (T2DM) are important risk factors for Alzheimer's disease (AD).
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Delivering drugs and agents to the brain is a huge challenge, especially for chronic neurodegenerative disorders, such as Alzheimer's disease (AD).
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Insulin resistance (IR) is a metabolic state preceding development of type 2 diabetes (DM2), cardiovascular disease, and neurodegenerative disorders, including Alzheimer's Disease (AD).
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Obesity and diabetes are both risk factors and consequences of psychiatric disorders.
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We report herein that wildtype, PSEN2 N141I and CRISPR/Cas9-corrected iPSC-derived BFCNs (and their precursors) show indistinguishable insulin signaling profiles as determined by the phosphorylation of canonical insulin signaling pathway molecules.
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47/100
Activation of microglia by classical inflammatory mediators can convert astrocytes into a neurotoxic A1 phenotype in a variety of neurological diseases 1,2 .
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Recent studies indicate that metabolic disorders such as diabetes and obesity are a major risk factor of psychiatric diseases.
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.
- Comparative effectiveness of glucagon-like peptide-1 agonists, dipeptidyl peptidase-4 inhibitors, and sulfonylureas on the risk of dementia in older individuals with type 2 diabetes in Sweden: an emulated trial study
- Val8-glucagon-like peptide-1 protects against Aβ1-40-induced impairment of hippocampal late-phase long-term potentiation and spatial learning in rats
- Glucagon-Like Peptide-1 Receptor Agonists and Risk of Parkinsonian Disorders in Patients with Obesity
- Parkinson's disease, insulin resistance and novel agents of neuroprotection
- Deciphering the Roles of Metformin in Alzheimer's Disease: A Snapshot
- Impairment of synaptic plasticity and memory formation in GLP-1 receptor KO mice: Interaction between type 2 diabetes and Alzheimer's disease
- Insulin, IGF-1 and GLP-1 signaling in neurodegenerative disorders: targets for disease modification?