Evidence map›Paper›PMID 33737866›Full record

ArticleFrontiers in cellular neuroscience2021

Molecular Mechanisms Underlying Synaptic and Axon Degeneration in Parkinson's Disease.

Nolwazi Z Gcwensa, Drèson L Russell, Rita M Cowell, Laura A Volpicelli-Daley

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
10.6field-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

65 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
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  10. Effects of α-synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  11. Review
  12. Single-cell sequencing: accurate disease detection.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  13. Article
  14. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

5 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.

Nolwazi Z GcwensaDepartment of Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, Civitan International Research Center, Birmingham, AL, United States.
Drèson L RussellDepartment of Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, Civitan International Research Center, Birmingham, AL, United States.
Rita M CowellDepartment of Neuroscience, Southern Research, Birmingham, AL, United States.
Laura A Volpicelli-DaleyDepartment of Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, Civitan International Research Center, Birmingham, AL, United States.
Civitan International · USSouthern Research Institute · US

Funding

Transcriptional regulation of metabolism in neuronsR01NS101958 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI COWELL, RITA MARIE · 2017 to 2021
$2.1M
Role of presynaptic targeting of alpha-synuclein in the pathogenesis of Parkinson's Disease and Dementia with Lewy BodiesR01NS102257 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI VOLPICELLI-DALEY, LAURA A. · 2018 to 2022
$1.9M
NINDS NIH HHS R01 NS101958NINDS NIH HHS R01 NS102257
6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease that impairs movement as well as causing multiple other symptoms such as autonomic dysfunction, rapid eye movement (REM) sleep behavior disorder, hyposmia, and cognitive changes. Loss of dopamine neurons in the substantia nigra pars compacta (SNc) and loss of dopamine terminals in the striatum contribute to characteristic motor features. Although therapies ease the symptoms of PD, there are no treatments to slow its progression. Accumulating evidence suggests that synaptic impairments and axonal degeneration precede neuronal cell body loss. Early synaptic changes may be a target to prevent disease onset and slow progression. Imaging of PD patients with radioligands, post-mortem pathologic studies in sporadic PD patients, and animal models of PD demonstrate abnormalities in presynaptic terminals as well as postsynaptic dendritic spines. Dopaminergic and excitatory synapses are substantially reduced in PD, and whether other neuronal subtypes show synaptic defects remains relatively unexplored. Genetic studies implicate several genes that play a role at the synapse, providing additional support for synaptic dysfunction in PD. In this review article we: (1) provide evidence for synaptic defects occurring in PD before neuron death; (2) describe the main genes implicated in PD that could contribute to synapse dysfunction; and (3) show correlations between the expression of

Indexed as

degenerationDementia with Lewy BodiesGWASParkinson’s diseasesynapseα-synuclein

Identifiers

PMID33737866
PMCPMC7960781
OpenAlexW3135528648

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.