Evidence map›Paper›PMID 27830778›Full record

ReviewNature2016

Defects in trafficking bridge Parkinson's disease pathology and genetics.

Asa Abeliovich, Aaron D Gitler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
260citing papers in PubMed, 3 pooled it
32.3field-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

260 citing papers in PubMed, 3 syntheses or guidelines pooled it, 464 citations in OpenAlex.

  1. Pooled it
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  20. A Common PD-RiskbioRxiv : the preprint server for biology · 2025
    Article

200 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

2 authors at 2 institutions in 1 country.

Asa AbeliovichDepartment of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA.
Aaron D GitlerDepartment of Genetics, Stanford University, Stanford, California 94305, USA.
Columbia University · USStanford University · US

Funding

US National Institute of Neurological Disorders and Stroke
6 · The paper itself

Abstract

Parkinson's disease is a debilitating, age-associated movement disorder. A central aspect of the pathophysiology of Parkinson's disease is the progressive demise of midbrain dopamine neurons and their axonal projections, but the underlying causes of this loss are unclear. Advances in genetics and experimental model systems have illuminated an important role for defects in intracellular transport pathways to lysosomes. The accumulation of altered proteins and damaged mitochondria, particularly at axon terminals, ultimately might overwhelm the capacity of intracellular disposal mechanisms. Cell-extrinsic mechanisms, including inflammation and prion-like spreading, are proposed to have both protective and deleterious functions in Parkinson's disease.

Indexed as

Parkinson Diseasealpha-SynucleinAnimalsBiological TransportEndocytosisGlucosylceramidaseHumansInflammationLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LysosomesModels, BiologicalMolecular Targeted TherapyNeuronsPrionsSynaptic Vesiclesalpha-SynucleinGlucosylceramidaseLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanPrions

Identifiers

PMID27830778
OpenAlexW2550736838

What OpenQuestion holds

Textmetadata
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.