Evidence map›Paper›PMID 20957078›Full record

ReviewASN neuro2010

Mitochondria and neuroplasticity.

Aiwu Cheng, Yan Hou, Mark P Mattson

Open access · goldAbstract readReview
In one paragraph

Review in ASN neuro, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 1 pooled it
5.4field-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

224 citing papers in PubMed, 1 synthesis or guideline pooled it, 424 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Chronic Exposure toInternational journal of molecular sciences · 2026
    Article
  6. Article
  7. Review
  8. GABA-Induced Exosomes Improve Memory Impairment in Aged Mice.International journal of molecular sciences · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

164 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 2 institutions in 1 country.

Aiwu ChengLaboratory of Neurosciences, National Institute of Aging Intramural Research Program, Baltimore, MD 21224, U.S.A. chengai@mail.nih.gov
Yan Hou
Mark P Mattson
Institute on Aging · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The production of neurons from neural progenitor cells, the growth of axons and dendrites and the formation and reorganization of synapses are examples of neuroplasticity. These processes are regulated by cell-autonomous and intercellular (paracrine and endocrine) programs that mediate responses of neural cells to environmental input. Mitochondria are highly mobile and move within and between subcellular compartments involved in neuroplasticity (synaptic terminals, dendrites, cell body and the axon). By generating energy (ATP and NAD(+)), and regulating subcellular Ca(2+) and redox homoeostasis, mitochondria may play important roles in controlling fundamental processes in neuroplasticity, including neural differentiation, neurite outgrowth, neurotransmitter release and dendritic remodelling. Particularly intriguing is emerging data suggesting that mitochondria emit molecular signals (e.g. reactive oxygen species, proteins and lipid mediators) that can act locally or travel to distant targets including the nucleus. Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke.

Indexed as

Alzheimer DiseaseAnimalsHumansMitochondriaNeurogenesisNeuronal PlasticityNeuronsParkinson DiseaseSynaptic TransmissionAD, Alzheimer's diseaseAP, adaptor proteinAPP, amyloid precursor proteinAβ, amyloid β-peptideBDNF, brain-derived neurotrophic factorCaMK, Ca2+/calmodulin-dependent protein kinaseCR, caloric restrictionCREB, cAMP-response-element-binding proteinES, embryonic stemETC, electron transport chainHD, Huntington's diseaseLRRK2, leucine-rich repeat kinase 2LTP, long-term potentiationMAPK, mitogen-activated protein kinasemitochondria biogenesismitochondria fission and fusionMn-SOD, manganese superoxide dismutaseneural progenitor cellNGF, nerve growth factorNMDA, N-methyl-d-aspartateNrf1, nuclear respiratory factor 1OPA1, Optic Atrophy-1PD, Parkinson's diseasePGC1α, peroxisome-proliferator-activated receptor γ co-activator 1αPINK1, PTEN (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1PPAR, peroxisome-proliferator-activated receptorUCP, uncoupling protein

Identifiers

PMID20957078
PMCPMC2949087
OpenAlexW2139780621

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.