Evidence map›Paper›PMID 21258649›Full record

ArticlePharmaceuticals (Basel, Switzerland)2010

Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases.

Lee J Martin

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
8.7field-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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 202 citations in OpenAlex.

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37 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

1 author at 1 institution in 1 country.

Lee J MartinDepartment of Pathology, Division of Neuropathology and Department of Neuroscience, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, Maryland 21205-2196, USA; martinl@jhmi.edu ; Tel.: +410-502-5170;
Johns Hopkins University · US

Funding

MECHANISMS OF NEURONAL APOPTOSIS IN VIVOR01AG016282 · NIA · JOHNS HOPKINS UNIVERSITY · PI MARTIN, LEE J · 2000 to 2009
$2.6M
MOTOR NEURON DEATH AND GLUTAMATE RECEPTORSR01NS034100 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MARTIN, LEE J · 1996 to 2006
$2.1M
Skeletal Muscle Mechanisms of Disease in ALSR01NS065895 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MARTIN, LEE J · 2010 to 2014
$1.7M
DNA Damage/Repair and Cell DeathR01NS052098 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MARTIN, LEE J · 2005 to 2009
$1.5M
NIA NIH HHS R01 AG016282NINDS NIH HHS R01 NS034100NINDS NIH HHS R01 NS052098NINDS NIH HHS R01 NS065895
6 · The paper itself

Abstract

Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS) are the most common human adult-onset neurodegenerative diseases. They are characterized by prominent age-related neurodegeneration in selectively vulnerable neural systems. Some forms of AD, PD, and ALS are inherited, and genes causing these diseases have been identified. Nevertheless, the mechanisms of the neuronal cell death are unresolved. Morphological, biochemical, genetic, as well as cell and animal model studies reveal that mitochondria could have roles in this neurodegeneration. The functions and properties of mitochondria might render subsets of selectively vulnerable neurons intrinsically susceptible to cellular aging and stress and overlying genetic variations, triggering neurodegeneration according to a cell death matrix theory. In AD, alterations in enzymes involved in oxidative phosphorylation, oxidative damage, and mitochondrial binding of Aβ and amyloid precursor protein have been reported. In PD, mutations in putative mitochondrial proteins have been identified and mitochondrial DNA mutations have been found in neurons in the substantia nigra. In ALS, changes occur in mitochondrial respiratory chain enzymes and mitochondrial cell death proteins. Transgenic mouse models of human neurodegenerative disease are beginning to reveal possible principles governing the biology of selective neuronal vulnerability that implicate mitochondria and the mitochondrial permeability transition pore. This review summarizes how mitochondrial pathobiology might contribute to neuronal death in AD, PD, and ALS and could serve as a target for drug therapy.

Identifiers

PMID21258649
PMCPMC3023298
OpenAlexW2090955970

What OpenQuestion holds

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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.