Evidence map›Paper›PMID 20563819›Full record

ReviewActa neuropathologica2010

The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia.

Walter J Schulz-Schaeffer

Registry-linked trialAbstract readReview
In one paragraph

Review in Acta neuropathologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02605161 (Imaging Blood Brain Imaging Dysfunction in Parkinson's Disease), which is not on this map. Cited by 326 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
326citing papers in PubMed, 3 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.

NCT02605161 completednot on this mapstarted 2015, after this paper: background citation

Imaging Blood Brain Imaging Dysfunction in Parkinson's Disease

TypeobservationalSponsorOttawa Hospital Research InstituteRan2015 to 2020Enrolled17ConditionsParkinson's Disease, Movement Disorders
3 · Its place in the literature

Who cites it

326 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Polymorphisms of the dopamine metabolic and signaling pathways are associated with susceptibility to motor levodopa-induced complications (MLIC) in Parkinson's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    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
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  17. Seeing Invisible Oligomers: Rethinking α-Synuclein Pathology Through Proximity Ligation Assay.Movement disorders : official journal of the Movement Disorder Society · 2026
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266 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

1 author.

Walter J Schulz-SchaefferDepartment of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, Göttingen, Germany. wjschulz@med.uni-goettingen.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are usually associated with loss of dopaminergic neurons. Loss of substantia nigra neurons and presence of Lewy body inclusions in some of the remaining neurons are the hallmark pathology seen in the final stages of the disease. Attempts to correlate Lewy body pathology to either cell death or severity of clinical symptoms, however, have not been successful. While the pathophysiology of the neurodegenerative process can hardly be explained by Lewy bodies, the clinical symptoms do indicate a degenerative process located at the presynapse resulting in a neurotransmitter deficiency. Recently it was shown that 90% or even more of alpha-synuclein aggregates in DLB cases were located at the presynapses in the form of very small deposits. In parallel, dendritic spines are retracted, whereas the presynapses are relatively preserved, suggesting a neurotransmitter deprivation. The same alpha-synuclein pathology can be demonstrated for PD. These findings give rise to the notion that not cell death but rather alpha-synuclein aggregate-related synaptic dysfunction causes the neurodegeneration. This opens new perspectives for understanding PD and DLB. If presynaptic alpha-synuclein aggregation, not neuronal loss, is the key issue of the neurodegenerative process, then PD and DLB may eventually be treatable in the future. The disease may progress via trans-synaptical spread, suggesting that stem cell transplants are of limited use. Future therapies may focus on the regeneration of synapses.

Indexed as

alpha-SynucleinAnimalsBrainLewy Body DiseaseParkinson DiseaseSynapsesalpha-Synuclein

Identifiers

PMID20563819
PMCPMC2892607

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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.