Evidence map›Paper›PMID 28382610›Full record

ReviewActa neurologica Taiwanica2016

The Role of Mitochondrial Aldehyde Dehydrogenase 2 (ALDH2) in Neuropathology and Neurodegeneration.

Che-Hong Chen, Amit U Joshi, Daria Mochly-Rosen

Open access · greenAbstract readReview
In one paragraph

Review in Acta neurologica Taiwanica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Association BetweenFrontiers in neurology · 2019
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. ALDH2 variance in disease and populations.Disease models & mechanisms · 2022
    Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Che-Hong ChenDepartment of Chemical and Systems Biology, Stanford University, School of Medicine, Stanford CA 94305-5174 USA.
Amit U JoshiDepartment of Chemical and Systems Biology, Stanford University, School of Medicine, Stanford CA 94305-5174 USA.
Daria Mochly-RosenDepartment of Chemical and Systems Biology, Stanford University, School of Medicine, Stanford CA 94305-5174 USA.
Stanford University · US

Funding

MECHANISMS OF ETHANOL-INDUCED CARDIAC PROTECTIONR01AA011147 · NIAAA · STANFORD UNIVERSITY · PI DARIA MOCHLY-ROSEN · 1996 to 2026
$8.2M
Mechanisms of Ethanol-Induced Cardiac ProtectionR37AA011147 · NIAAA · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 2009 to 2018
$5.3M
NIAAA NIH HHS R01 AA011147NIAAA NIH HHS R37 AA011147
6 · The paper itself

Abstract

Aldehydes-induced toxicity has been implicated in many neurodegenerative diseases. Exposure to reactive aldehydes from (1) alcohol and food metabolism; (2) environmental pollutants, including car, factory exhausts, smog, pesticides, herbicides; (3) metabolism of neurotransmitters, amino acids and (4) lipid peroxidation of biological membrane from excessive ROS, all contribute to 'aldehydic load' that has been linked to the pathology of neurodegenerative diseases. In particular, the α, β-unsaturated aldehydes derived from lipid peroxidation, 4-hydroxynonenal (4-HNE), DOPAL (MAO product of dopamine), malondialdehyde, acrolein and acetaldehyde, all readily form chemical adductions with proteins, DNA and lipids, thus causing neurotoxicity. Mitochondrial aldehyde dehydrogenase 2 (ALDH 2) is a major aldehyde metabolizing enzyme that protects against deleterious aldehyde buildup in brain, a tissue that has a particularly high mitochondrial content. In this review, we highlight the deleterious effects of increased aldehydic load in the neuropathology of ischemic stroke, Alzheimer's disease and Parkinson's disease. We also discuss evidence for the association between ALDH2 deficiency, a common East Asianspecific mutation, and these neuropathologies. A novel class of small molecule aldehyde dehydrogenase activators (Aldas), represented by Alda-1, reduces neuronal cell death in models of ischemic stroke, Alzheimer's disease and Parkinson's disease. Together, these data suggest that reducing aldeydic load by enhancing the activity of aldehyde dehydrogenases, such as ALDH2, represents as a therapeutic strategy for neurodegenerative diseases.

Indexed as

Aldehyde Dehydrogenase, MitochondrialAldehydesAlzheimer DiseaseBrain IschemiaHumansParkinson DiseaseAldehyde Dehydrogenase, MitochondrialAldehydesALDH2 protein, human

Identifiers

PMID28382610
PMCPMC10618051
OpenAlexW2748525150

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.