ReviewNeuropharmacology2018
Amylin in Alzheimer's disease: Pathological peptide or potential treatment?
Review in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- The Insulin Sensitizer KBP-336 Prevents Diabetes-Induced Cognitive decline in ZDF Rats.The journal of prevention of Alzheimer's disease · 2024Article
- Repositioning of Anti-Diabetic Drugs against Dementia: Insight from Molecular Perspectives to Clinical Trials.International journal of molecular sciences · 2023Review
- Integrated DNA Methylation/RNA Profiling in Middle Temporal Gyrus of Alzheimer's Disease.Cellular and molecular neurobiology · 2023Article
- Amylin and Secretases in the Pathology and Treatment of Alzheimer's Disease.Biomolecules · 2022Review
- Mediators of Amylin Action in Metabolic Control.Journal of clinical medicine · 2022Review
- The Effect of Nutrients on Alzheimer's Disease Biomarkers: A Metabolomic Approach.Advances in experimental medicine and biology · 2021Article
- Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing.Nature reviews. Drug discovery · 2020Review
- Involvement of amylin B-H2S-connexin 43 signaling pathway in vascular dysfunction and enhanced ischemia-reperfusion-induced myocardial injury in diabetic rats.Bioscience reports · 2020Article
- High-Speed Atomic Force Microscopy Reveals the Structural Dynamics of the Amyloid-β and Amylin Aggregation Pathways.International journal of molecular sciences · 2020Review
- Islet Amyloid Polypeptide: A Partner in Crime With Aβ in the Pathology of Alzheimer's Disease.Frontiers in molecular neuroscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease for which we currently lack effective treatments or a cure. The pancreatic peptide hormone amylin has recently garnered interest as a potential pharmacological target for the treatment of AD. A number of studies have demonstrated that amylin and amylin analogs like the FDA-approved diabetes drug pramlintide can reduce amyloid burden in the brain and improve cognitive symptoms of AD. However, other data suggest that amylin may have pathological effects in AD due to its propensity to misfold and aggregate under certain conditions. Here, the literature supporting a beneficial versus harmful role of amylin in AD is reviewed. Additionally, several critical gaps in the literature are discussed, such as our limited understanding of the amylin system during aging and in disease states, as well as complexities of amylin receptor signaling and of changing pathophysiology during AD progression that might underlie the seemingly conflicting or contradictory results in the amylin/AD literature. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'
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What OpenQuestion holds
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.