Evidence map›Paper›PMID 37881206›Full record

ReviewCurrent developments in nutrition2023

Creatine as a Therapeutic Target in Alzheimer's Disease.

Aaron N Smith, Jill K Morris, Aaron F Carbuhn, Trent J Herda, Jessica E Keller, Debra K Sullivan, Matthew K Taylor

Open access · goldAbstract readReview
In one paragraph

Review in Current developments in nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Effects of the SGLT2 inhibitor dapagliflozin in early Alzheimer's disease: A randomized controlled trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

7 authors at 2 institutions in 1 country.

Aaron N SmithDepartment of Dietetics and Nutrition, University of Kansas Medical Center, Kansas City, KS, United States.
Jill K MorrisAlzheimer's Disease Research Center, University of Kansas, Fairway, KS, United States.
Aaron F CarbuhnDepartment of Dietetics and Nutrition, University of Kansas Medical Center, Kansas City, KS, United States.
Trent J HerdaDepartment of Health, Sport, and Exercise Sciences, University of Kansas, Lawrence, KS, United States.
Jessica E KellerDepartment of Dietetics and Nutrition, University of Kansas Medical Center, Kansas City, KS, United States.
Debra K SullivanDepartment of Dietetics and Nutrition, University of Kansas Medical Center, Kansas City, KS, United States.
Matthew K TaylorDepartment of Dietetics and Nutrition, University of Kansas Medical Center, Kansas City, KS, United States.
University of Kansas · USUniversity of Kansas Medical Center · US

Funding

Acute exercise and the cerebral metabolic response in aging and Alzheimer's DiseaseR01AG062548 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MORRIS, JILL KATHLEEN · 2020 to 2024
$2.4M
High Glycemic Diet and Alzheimer's RiskK01AG065487 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI TAYLOR, MATTHEW · 2020 to 2024
$654k
NIA NIH HHS K01 AG065487NIA NIH HHS R01 AG062548
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease, affecting approximately 6.5 million older adults in the United States. Development of AD treatment has primarily centered on developing pharmaceuticals that target amyloid-β (Aβ) plaques in the brain, a hallmark pathological biomarker that precedes symptomatic AD. Though recent clinical trials of novel drugs that target Aβ have demonstrated promising preliminary data, these pharmaceuticals have a poor history of developing into AD treatments, leading to hypotheses that other therapeutic targets may be more suitable for AD prevention and treatment. Impaired brain energy metabolism is another pathological hallmark that precedes the onset of AD that may provide a target for intervention. The brain creatine (Cr) system plays a crucial role in maintaining bioenergetic flux and is disrupted in AD. Recent studies using AD mouse models have shown that supplementing with Cr improves brain bioenergetics, as well as AD biomarkers and cognition. Despite these promising findings, no human trials have investigated the potential benefits of Cr supplementation in AD. This narrative review discusses the link between Cr and AD and the potential for Cr supplementation as a treatment for AD.

Indexed as

Alzheimer’s diseasebioenergeticsbraincreatinemitochondria

Identifiers

PMID37881206
PMCPMC10594571
OpenAlexW4387159152

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.