Evidence map›Paper›PMID 22329649›Full record

ReviewCurrent Alzheimer research2012

Metabolic dysfunction in Alzheimer's disease and related neurodegenerative disorders.

Huan Cai, Wei-na Cong, Sunggoan Ji, Sarah Rothman, Stuart Maudsley, Bronwen Martin

Abstract readReview
In one paragraph

Review in Current Alzheimer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

168 citing papers in PubMed, 313 citations in OpenAlex.

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  17. G protein-coupled receptor digital twins for precision and personalized medicine.Computational and structural biotechnology journal · 2025
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108 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Huan CaiMetabolism Unit, National Institute on Aging, Baltimore, MD 21224, USA.
Wei-na Cong
Sunggoan Ji
Sarah Rothman
Stuart Maudsley
Bronwen Martin
National Institute on Aging · US

Funding

Oxidative stresses and complex proteomic responses to themZIAAG000325 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.4M
Age and pathology-induced alteration of G protein-coupled receptor signalingZIAAG000318 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.0M
Innate intelligence and prognostication for prevention of neurodegenerationZIAAG000319 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.0M
Cognitive function and metabolic controlZIAAG000917 · NIA · NATIONAL INSTITUTE ON AGING · PI MARTIN, BRONWEN · 2010 to 2012
$901k
A systems biology approach for assessing metabolic alterations across life-spanZIAAG000915 · NIA · NATIONAL INSTITUTE ON AGING · PI MARTIN, BRONWEN · 2010 to 2012
$548k
Development of novel methods for systems biology of metabolism and agingZIAAG000916 · NIA · NATIONAL INSTITUTE ON AGING · PI MARTIN, BRONWEN · 2010 to 2012
$518k
Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000917
6 · The paper itself

Abstract

Alzheimer's disease and other related neurodegenerative diseases are highly debilitating disorders that affect millions of people worldwide. Efforts towards developing effective treatments for these disorders have shown limited efficacy at best, with no true cure to this day being present. Recent work, both clinical and experimental, indicates that many neurodegenerative disorders often display a coexisting metabolic dysfunction which may exacerbate neurological symptoms. It stands to reason therefore that metabolic pathways may themselves contain promising therapeutic targets for major neurodegenerative diseases. In this review, we provide an overview of some of the most recent evidence for metabolic dysregulation in Alzheimer's disease, Huntington's disease, and Parkinson's disease, and discuss several potential mechanisms that may underlie the potential relationships between metabolic dysfunction and etiology of nervous system degeneration. We also highlight some prominent signaling pathways involved in the link between peripheral metabolism and the central nervous system that are potential targets for future therapies, and we will review some of the clinical progress in this field. It is likely that in the near future, therapeutics with combinatorial neuroprotective and 'eumetabolic' activities may possess superior efficacies compared to less pluripotent remedies.

Indexed as

AdiponectinAlzheimer DiseaseBody WeightBrain-Derived Neurotrophic FactorGhrelinGlucagon-Like Peptide 1GlucoseHumansLeptinMetabolic DiseasesNeurodegenerative DiseasesAdiponectinBrain-Derived Neurotrophic FactorGhrelinGlucagon-Like Peptide 1GlucoseLeptin

Identifiers

PMID22329649
PMCPMC4097094
OpenAlexW48248669

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.