Evidence map›Paper›PMID 37475056›Full record

ReviewMolecular neurodegeneration2023

Axonal energy metabolism, and the effects in aging and neurodegenerative diseases.

Sen Yang, Jung Hyun Park, Hui-Chen Lu

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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2 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

3 authors at 1 institution in 1 country.

Sen YangThe Linda and Jack Gill Center for Biomolecular Sciences, Indiana University, Bloomington, IN, 47405, USA.
Jung Hyun ParkThe Linda and Jack Gill Center for Biomolecular Sciences, Indiana University, Bloomington, IN, 47405, USA.
Hui-Chen LuThe Linda and Jack Gill Center for Biomolecular Sciences, Indiana University, Bloomington, IN, 47405, USA. hclu@indiana.edu.ORCID 0000-0002-6628-7177
Indiana University Bloomington · US

Funding

Molecular and genetic studies of NMNAT2 in neuroprotectionR01NS086794 · NINDS · TRUSTEES OF INDIANA UNIVERSITY · PI LU, HUI-CHEN · 2014 to 2025
$5.0M
NINDS NIH HHS NS086794NINDS NIH HHS R01 NS086794
6 · The paper itself

Abstract

Human studies consistently identify bioenergetic maladaptations in brains upon aging and neurodegenerative disorders of aging (NDAs), such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and Amyotrophic lateral sclerosis. Glucose is the major brain fuel and glucose hypometabolism has been observed in brain regions vulnerable to aging and NDAs. Many neurodegenerative susceptible regions are in the topological central hub of the brain connectome, linked by densely interconnected long-range axons. Axons, key components of the connectome, have high metabolic needs to support neurotransmission and other essential activities. Long-range axons are particularly vulnerable to injury, neurotoxin exposure, protein stress, lysosomal dysfunction, etc. Axonopathy is often an early sign of neurodegeneration. Recent studies ascribe axonal maintenance failures to local bioenergetic dysregulation. With this review, we aim to stimulate research in exploring metabolically oriented neuroprotection strategies to enhance or normalize bioenergetics in NDA models. Here we start by summarizing evidence from human patients and animal models to reveal the correlation between glucose hypometabolism and connectomic disintegration upon aging/NDAs. To encourage mechanistic investigations on how axonal bioenergetic dysregulation occurs during aging/NDAs, we first review the current literature on axonal bioenergetics in distinct axonal subdomains: axon initial segments, myelinated axonal segments, and axonal arbors harboring pre-synaptic boutons. In each subdomain, we focus on the organization, activity-dependent regulation of the bioenergetic system, and external glial support. Second, we review the mechanisms regulating axonal nicotinamide adenine dinucleotide (NAD

Indexed as

Neurodegenerative DiseasesAgingAnimalsAxonsEnergy MetabolismGlucoseHumansNADGlucoseNADAgingAxonal bioenergeticsAxonopathyEnergy metabolismGlucoseGlycolysisMitochondriaNADNeurodegenerationNeuroprotection

Identifiers

PMID37475056
PMCPMC10357692
OpenAlexW4384925673

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.