ArticleNeuropharmacology2017
Amylin receptor ligands reduce the pathological cascade of Alzheimer's disease.
Article in Neuropharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Effect of antidiabetic drugs in Alzheimer´s disease: a systematic review of preclinical and clinical studies.Molecular neurodegeneration · 2025Pooled it
- Cross-seeding of IAPP and Aβ42: A review of the molecular link between type 2 diabetes and Alzheimer's disease.Metabolic brain disease · 2025Review
- Identification of Associations Between Peripheral Blood Gene Expression and Cerebrospinal Fluid Biomarkers in Alzheimer's Disease Using an Improved Joint Multi-Task Sparse Canonical Correlation Analysis Algorithm.Applied biochemistry and biotechnology · 2025Article
- Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025Review
- Enhancing Stability and Bioavailability of Peptidylglycine Alpha-Amidating Monooxygenase in Circulation for Clinical Use.Biomolecules · 2025Article
- Inhibition of Indoleamine 2,3-Dioxygenase Exerts Antidepressant-like Effects through Distinct Pathways in Prelimbic and Infralimbic Cortices in Rats under Intracerebroventricular Injection with Streptozotocin.International journal of molecular sciences · 2024Article
- Cellular Stress Response (Hormesis) in Response to Bioactive Nutraceuticals with Relevance to Alzheimer Disease.Antioxidants & redox signaling · 2023Review
- Novel Hominid-Specific IAPP Isoforms: Potential Biomarkers of Early Alzheimer's Disease and Inhibitors of Amyloid Formation.Biomolecules · 2023Article
- Amylin and Secretases in the Pathology and Treatment of Alzheimer's Disease.Biomolecules · 2022Review
- Amylin Pharmacology in Alzheimer's Disease Pathogenesis and Treatment.Current neuropharmacology · 2022Review
- Role of Receptors in Relation to Plaques and Tangles in Alzheimer's Disease Pathology.International journal of molecular sciences · 2021Review
- Genetic Depletion of Amylin/Calcitonin Receptors Improves Memory and Learning in Transgenic Alzheimer's Disease Mouse Models.Molecular neurobiology · 2021Article
- Review
- High-Speed Atomic Force Microscopy Reveals the Structural Dynamics of the Amyloid-β and Amylin Aggregation Pathways.International journal of molecular sciences · 2020Review
- The Importance of Understanding Amylin Signaling Mechanisms for Therapeutic Development in the Treatment of Alzheimer's Disease.Current pharmaceutical design · 2020Review
- Association of Plasma Amylin Concentration With Alzheimer Disease and Brain Structure in Older Adults.JAMA network open · 2019Article
- Activation of amylin receptors attenuates alcohol-mediated behaviours in rodents.Addiction biology · 2019Article
- Levels of islet amyloid polypeptide in cerebrospinal fluid and plasma from patients with Alzheimer's disease.PloS one · 2019Article
- Amylin Signaling in Diabetes and Alzheimer's Disease: Therapy or Pathology?Journal of neurology & neuromedicine · 2019Article
- Effects of Amylin Against Amyloid-β-Induced Tauopathy and Synapse Loss in Primary Neurons.Journal of Alzheimer's disease : JAD · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Amylin is an important gut-brain axis hormone. Since amylin and amyloid-β peptide (Aβ) share similar β sheet secondary structure despite not having the same primary sequences, we hypothesized that the accumulation of Aβ in the brains of subjects with Alzheimer's disease (AD) might compete with amylin for binding to the amylin receptor (AmR). If true, adding exogenous amylin type peptides would compete with Aβ and reduce the AD pathological cascade, improving cognition. Here we report that a 10-week course of peripheral treatment with human amylin significantly reduced multiple different markers associated with AD pathology, including reducing levels of phospho-tau, insoluble tau, two inflammatory markers (Iba1 and CD68), as well as cerebral Aβ. Amylin treatment also led to improvements in learning and memory in two AD mouse models. Mechanistic studies showed that an amylin receptor antagonist successfully antagonized some protective effects of amylin in vivo, suggesting that the protective effects of amylin require interaction with its cognate receptor. Comparison of signaling cascades emanating from AmR suggest that amylin electively suppresses activation of the CDK5 pathway by Aβ. Treatment with amylin significantly reduced CDK5 signaling in a receptor dependent manner, dramatically decreasing the levels of p25, the active form of CDK5 with a corresponding reduction in tau phosphorylation. This is the first report documenting the ability of amylin treatment to reduce tauopathy and inflammation in animal models of AD. The data suggest that the clinical analog of amylin, pramlintide, might exhibit utility as a therapeutic agent for AD and other neurodegenerative diseases.
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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.