Evidence map›Paper›PMID 36708219›Full record

ReviewMolecular nutrition & food research2024

Type-2 Diabetes, Pancreatic Amylin, and Neuronal Metabolic Remodeling in Alzheimer's Disease.

Noah Leibold, James R Bain, Florin Despa

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular nutrition & food research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Noah LeiboldDepartment of Pharmacology and Nutritional Sciences, The University of Kentucky, Lexington, KY, 40506, USA.ORCID 0000-0001-7737-0382
James R BainDivision of Endocrinology, Metabolism, and Nutrition, Department of Medicine, Claude D. Pepper Older Americans Independence Center, and Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, 27710, USA.
Florin DespaDepartment of Pharmacology and Nutritional Sciences, The University of Kentucky, Lexington, KY, 40506, USA.ORCID 0000-0002-5879-6449
University of Kentucky · USDuke University · US

Funding

Resource Core 3 - Metabolomics CoreP30AG028716 · NIA · DUKE UNIVERSITY · PI Virginia B Kraus · 2006 to 2026
$24.6M
Pilot & Feasibility ProgramP30DK124723 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Morgana Lee Mongraw-Chaffin · 2020 to 2026
$11.0M
The Amylin Dyshomeostasis Hypothesis of Vascular Contributions to Cognitive Impairment and Dementia (VCID)R01NS116058 · NINDS · UNIVERSITY OF KENTUCKY · PI DESPA, FLORIN · 2020 to 2024
$3.8M
Programming amylin secretion to slow brain aging - an animal modelR01AG057290 · NIA · UNIVERSITY OF KENTUCKY · PI DESPA, FLORIN, THINAKARAN, GOPAL · 2017 to 2021
$3.3M
Predicting Newborn and Childhood Adiposity: An Integrated Omics ApproachR01DK117491 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LOWE, WILLIAM L, SCHOLTENS, DENISE M · 2018 to 2022
$2.8M
Biomarkers of Dietary Intake and Exposure Data Coordinating CenterU24DK129557 · NIDDK · DUKE UNIVERSITY · PI CHAKRABORTY, HRISHIKESH · 2021 to 2025
$2.6M
Role of Systemic Amylin Dyshomeostasis in Alzheimer's DiseaseR01AG053999 · NIA · UNIVERSITY OF KENTUCKY · PI DESPA, FLORIN · 2016 to 2020
$1.9M
NIA NIH HHS 2P30AG028716NIA NIH HHS AG053999NIA NIH HHS AG057290NIA NIH HHS P30 AG028716NIA NIH HHS R01 AG053999NIA NIH HHS R01 AG057290NIDDK NIH HHS P30 DK124723NIDDK NIH HHS R01 DK117491NIDDK NIH HHS U24 DK129557NINDS NIH HHS NS116058NINDS NIH HHS R01 NS116058
6 · The paper itself

Abstract

Type-2 diabetes raises the risk for Alzheimer's disease (AD)-type dementia and the conversion from mild cognitive impairment to dementia, yet mechanisms connecting type-2 diabetes to AD remain largely unknown. Amylin, a pancreatic β-cell hormone co-secreted with insulin, participates in the central regulation of satiation, but also forms pancreatic amyloid in persons with type-2 diabetes and synergistically interacts with brain amyloid β (Aβ) pathology, in both sporadic and familial Alzheimer's disease (AD). Growing evidence from studies of tumor growth, together with early observations in skeletal muscle, indicates amylin as a potential trigger of cellular metabolic reprogramming. Because the blood, cerebrospinal fluid, and brain parenchyma in humans with AD have increased concentrations of amylin, amylin-mediated pathological processes in the brain may involve neuronal metabolic remodeling. This review summarizes recent progress in understanding the link between prediabetic hypersecretion of amylin and risk of neuronal metabolic remodeling and AD and suggests nutritional and medical effects of food constituents that might prevent and/or ameliorate amylin-mediated neuronal metabolic remodeling.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2Islet Amyloid PolypeptideNeuronsAmyloid beta-PeptidesAnimalsBrainHumansAmyloid beta-PeptidesIslet Amyloid PolypeptideAlzheimer's diseaseamylindiabetesmetabolismvascular cognitive impairment and dementia (VCID)

Identifiers

PMID36708219
PMCPMC10374875
OpenAlexW4318391110

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.