Evidence map›Paper›PMID 28104909›Full record

ReviewNature reviews. Neuroscience2017

Selective neuronal vulnerability in Parkinson disease.

D James Surmeier, José A Obeso, Glenda M Halliday

Abstract readReview
In one paragraph

Review in Nature reviews. Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 619 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
619citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

619 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  5. Article
  6. Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026
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  18. Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026
    Review
  19. Review
  20. Article

559 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

3 authors.

D James SurmeierDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
José A ObesoCentro Integral de Neurociencias A.C. (CINAC), HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU San Pablo University, 28938 Madrid, Spain.
Glenda M HallidayBrain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney 2006, Australia.

Funding

SYNAPTIC CONTROLOF PALLIDAL ACTIVITYP50NS047085 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KRAINC, DIMITRI · 2003 to 2018
$19.2M
NINDS NIH HHS P50 NS047085
6 · The paper itself

Abstract

Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal dysfunction and death. However, post-mortem analysis of human brains and connectome-mapping studies show that the pattern of LP in cPD is not consistent with this simple model, arguing that, if LP propagates in cPD, it must be gated by cell- or region-autonomous mechanisms. Moreover, the correlation between LP and neuronal death is weak. In this Review, we briefly discuss the evidence for and against the spreading LP model, as well as evidence that cell-autonomous factors govern both α-syn pathology and neuronal death.

Indexed as

Cell Deathalpha-SynucleinAnimalsBrainHumansLewy BodiesNeuronsParkinson Diseasealpha-Synuclein

Identifiers

PMID28104909
PMCPMC5564322

What OpenQuestion holds

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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.