Evidence map›Paper›PMID 27923524›Full record

ReviewNutrition research (New York, N.Y.)2016

The therapeutic potential of metabolic hormones in the treatment of age-related cognitive decline and Alzheimer's disease.

John Grizzanti, Hyoung-Gon Lee, Antoni Camins, Merce Pallas, Gemma Casadesus

Open access · greenAbstract readReview
In one paragraph

Review in Nutrition research (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. 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

5 authors at 3 institutions in 2 countries.

John GrizzantiSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Hyoung-Gon LeeDepartment of Biology, University of Texas, San Antonio, TX, USA.
Antoni CaminsDepartment of Pharmacology and Therapeutic Chemistry, Universitat de Barcelona, Barcelona, Spain.
Merce PallasDepartment of Pharmacology and Therapeutic Chemistry, Universitat de Barcelona, Barcelona, Spain.
Gemma CasadesusSchool of Biomedical Sciences, Kent State University, Kent, OH, USA; Department of Biological Sciences, Kent State University, Kent, OH, USA. Electronic address: Gcasades@kent.edu.
Kent State University · USUniversitat de Barcelona · ESThe University of Texas at San Antonio · US

Funding

Mechanisms of Metabolic Hormone Amylin Action on Alzheimer's Disease PathogenesisR15AG050292 · NIA · KENT STATE UNIVERSITY · PI CASADESUS, GEMMA · 2016 to 2016
$444k
NIA NIH HHS R15 AG050292
6 · The paper itself

Abstract

Aging leads to a number of physiological alterations, specifically changes in circulating hormone levels, increases in fat deposition, decreases in metabolism, changes in inflammatory responses, and reductions in growth factors. These progressive changes in physiology and metabolism are exacerbated by modern culture and Western diet and give rise to diseases such as obesity, metabolic syndrome, and type 2 (non-insulin-dependent) diabetes (T2D). These age and lifestyle-related metabolic diseases are often accompanied by insulin and leptin resistance, as well as aberrant amylin production and signaling. Many of these alterations in hormone production and signaling are directly influenced by an increase in both oxidative stress and inflammation. Importantly, changes in hormone production and signaling have direct effects on brain function and the development of age-related neurologic disorders. Therefore, this review aims to present evidence on the effects that diet and metabolic disease have on age-related cognitive decline and the development of cognitive diseases, particularly Alzheimer disease. This review will focus on the metabolic hormones insulin, leptin, and amylin and their role in cognitive decline, as well as the therapeutic potential of these hormones in treating cognitive disease. Future investigations targeting the long-term effects of insulin and leptin treatment may reveal evidence to reduce risk of cognitive decline and Alzheimer disease.

Indexed as

AgingAlzheimer DiseaseCognitionCognitive DysfunctionDiabetes Mellitus, Type 2HumansInsulinIslet Amyloid PolypeptideLeptinObesityInsulinIslet Amyloid PolypeptideLeptinAlzheimer diseaseAmylinDiabetesInsulinLeptinObesity

Identifiers

PMID27923524
PMCPMC5490446
OpenAlexW2554647729

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.