Evidence map›Paper›PMID 24325796›Full record

ArticleNeurobiology of aging2014

Mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice.

Lee J Martin, Samantha Semenkow, Allison Hanaford, Margaret Wong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
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  5. Unravelling the novel insights between miR-7 and Parkinson's disease (PD).Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
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  16. Article
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  19. α-Synuclein and biological membranes: the danger of loving too much.Chemical communications (Cambridge, England) · 2023
    Review
  20. Review

14 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

4 authors at 2 institutions in 1 country.

Lee J MartinDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: martinl@jhmi.edu.
Samantha SemenkowDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Allison HanafordDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Margaret WongDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USJohns Hopkins Medicine · 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
DNA Damage/Repair and Cell DeathR01NS052098 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MARTIN, LEE J · 2005 to 2009
$1.5M
NIA NIH HHS AG016282NIA NIH HHS R01 AG016282NINDS NIH HHS NS034100NINDS NIH HHS NS052098NINDS NIH HHS R01 NS034100NINDS NIH HHS R01 NS052098
6 · The paper itself

Abstract

Parkinson's disease (PD) is a movement disorder caused by neurodegeneration in neocortex, substantia nigra and brainstem, and synucleinopathy. Some inherited PD is caused by mutations in α-synuclein (αSyn), and inherited and idiopathic PD is associated with mitochondrial perturbations. However, the mechanisms of pathogenesis are unresolved. We characterized a human αSyn transgenic mouse model and tested the hypothesis that the mitochondrial permeability transition pore (mPTP) is involved in the disease mechanisms. C57BL/6 mice expressing human A53T-mutant αSyn driven by a thymic antigen-1 promoter develop a severe, age-related, fatal movement disorder involving ataxia, rigidity, and postural instability. These mice develop synucleinopathy and neocortical, substantia nigra, and cerebello-rubro-thalamic degeneration involving mitochondriopathy and apoptotic and non-apoptotic neurodegeneration. Interneurons undergo apoptotic degeneration in young mice. Mutant αSyn associated with dysmorphic neuronal mitochondria and bound voltage-dependent anion channels. Genetic ablation of cyclophilin D, an mPTP modulator, delayed disease onset, and extended lifespans of mutant αSyn mice. Thus, mutant αSyn transgenic mice on a C57BL/6 background develop PD-like phenotypes, and the mPTP is involved in their disease mechanisms.

Indexed as

alpha-SynucleinAnimalsDisease Models, AnimalMiceMice, Inbred C57BLMice, TransgenicMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMutationParkinson Diseasealpha-SynucleinMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreAdenine nucleotide translocaseCerebellumInterneuronPorinPpifVoltage-dependent anion channel 1

Identifiers

PMID24325796
PMCPMC3948207
OpenAlexW2093343889

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.