Evidence map›Paper›PMID 22735187›Full record

ReviewThe EMBO journal2012

Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences.

Nicole Exner, Anne Kathrin Lutz, Christian Haass, Konstanze F Winklhofer

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03840005 (A Phase II, Placebo Controlled, Double Blind, Randomised Clinical Trial To Assess The Safety And Tolerability Of 30mg/kg Daily Ursodeoxycholic Acid), which is not on this map. Cited by 315 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
315citing papers in PubMed, 4 pooled it
40.9field-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.

NCT03840005 phase2completednot on this mapstarted 2018, after this paper: background citation

A Phase II, Placebo Controlled, Double Blind, Randomised Clinical Trial To Assess The Safety And Tolerability Of 30mg/kg Daily Ursodeoxycholic Acid (UDCA) In Patients With Parkinson's Disease (PD)

TypeinterventionalSponsorSheffield Teaching Hospitals NHS Foundation TrustRan2018 to 2021Enrolled31ConditionsParkinson's DiseaseArmsUrsonorm
3 · Its place in the literature

Who cites it

315 citing papers in PubMed, 4 syntheses or guidelines pooled it, 616 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. A systematic review of molecular approaches that link mitochondrial dysfunction and neuroinflammation in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  4. Pooled it
  5. Trial
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  20. Molecular mirror: reflecting the complexity of Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review

255 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 1 institution in 1 country.

Nicole ExnerBiochemistry, Adolf Butenandt Institute, Ludwig Maximilians University, Munich, Germany.
Anne Kathrin Lutz
Christian Haass
Konstanze F Winklhofer
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons are critically dependent on mitochondrial integrity based on specific morphological, biochemical, and physiological features. They are characterized by high rates of metabolic activity and need to respond promptly to activity-dependent fluctuations in bioenergetic demand. The dimensions and polarity of neurons require efficient transport of mitochondria to hot spots of energy consumption, such as presynaptic and postsynaptic sites. Moreover, the postmitotic state of neurons in combination with their exposure to intrinsic and extrinsic neuronal stress factors call for a high fidelity of mitochondrial quality control systems. Consequently, it is not surprising that mitochondrial alterations can promote neuronal dysfunction and degeneration. In particular, mitochondrial dysfunction has long been implicated in the etiopathogenesis of Parkinson's disease (PD), based on the observation that mitochondrial toxins can cause parkinsonism in humans and animal models. Substantial progress towards understanding the role of mitochondria in the disease process has been made by the identification and characterization of genes causing familial variants of PD. Studies on the function and dysfunction of these genes revealed that various aspects of mitochondrial biology appear to be affected in PD, comprising mitochondrial biogenesis, bioenergetics, dynamics, transport, and quality control.

Indexed as

AnimalsHumansMitochondriaNeuronsParkinson Disease

Identifiers

PMID22735187
PMCPMC3400019
OpenAlexW2109326232

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.