Evidence map›Paper›PMID 26883165›Full record

ReviewBrain research2016

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress.

Mohammed Akbar, Musthafa Mohamed Essa, Ghazi Daradkeh, Mohamed A Abdelmegeed, Youngshim Choi, Lubna Mahmood, Byoung-Joon Song

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
8.4field-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

84 citing papers in PubMed, 174 citations in OpenAlex.

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24 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

7 authors at 4 institutions in 3 countries.

Mohammed AkbarSection of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Musthafa Mohamed EssaDepartment of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Oman; Ageing and Dementia Research Group, Sultan Qaboos University, Oman.
Ghazi DaradkehDepartment of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Oman.
Mohamed A AbdelmegeedSection of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Youngshim ChoiSection of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Lubna MahmoodDepartment of Nutritional Sciences, Qatar University, Qatar.
Byoung-Joon SongSection of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
National Institute on Alcohol Abuse and Alcoholism · USSultan Qaboos University · OMNational Institutes of Health · USQatar University · QA

Funding

Alcohol Metabolism, Functional Consequences, Apoptosis Signaling Pathways, and Organ DamageZIAAA000036 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI SONG, BYOUNG-JOON · 2009 to 2025
$14.8M
Intramural NIH HHS Z99 AA999999
6 · The paper itself

Abstract

Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities.

Indexed as

Age FactorsAntioxidantsApoptosisDNA, MitochondrialGlutamic AcidHumansLipid MetabolismMitochondriaMitochondrial ProteinsNeurodegenerative DiseasesOxidation-ReductionOxidative StressReactive Oxygen SpeciesAntioxidantsDNA, MitochondrialGlutamic AcidMitochondrial ProteinsReactive Oxygen SpeciesAntioxidantsMitochondrial dysfunctionNeurodegenerative diseasesNeuronal cell deathOxidative stressPost-translational protein modificationsTranslational research

Identifiers

PMID26883165
PMCPMC4821765
OpenAlexW2263878260

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.