Evidence map›Paper›PMID 38203531›Full record

ReviewInternational journal of molecular sciences2023

Alpha-Synuclein Contribution to Neuronal and Glial Damage in Parkinson's Disease.

Kamil Saramowicz, Natalia Siwecka, Grzegorz Galita, Aleksandra Kucharska-Lusina, Wioletta Rozpędek-Kamińska, Ireneusz Majsterek

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
11.1field-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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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  5. Neuroprotective Potential of Synaptamide in MPTP-Induced Parkinson's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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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

6 authors at 1 institution in 1 country.

Kamil SaramowiczDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0009-0000-0395-5986
Natalia SiweckaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0002-0308-580X
Grzegorz GalitaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0002-1559-2796
Aleksandra Kucharska-LusinaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.
Wioletta Rozpędek-KamińskaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0001-9206-1203
Ireneusz MajsterekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland.
Medical University of Lodz · PL

Funding

Medical University of Lodz 503/1-156-07/503-11-001National Science Center 2016/21/B/NZ5/01411National Science Center 2021/43/O/NZ5/02068
6 · The paper itself

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disease characterized by the progressive loss of dopaminergic neurons in the substantia nigra and the widespread accumulation of alpha-synuclein (αSyn) protein aggregates. αSyn aggregation disrupts critical cellular processes, including synaptic function, mitochondrial integrity, and proteostasis, which culminate in neuronal cell death. Importantly, αSyn pathology extends beyond neurons-it also encompasses spreading throughout the neuronal environment and internalization by microglia and astrocytes. Once internalized, glia can act as neuroprotective scavengers, which limit the spread of αSyn. However, they can also become reactive, thereby contributing to neuroinflammation and the progression of PD. Recent advances in αSyn research have enabled the molecular diagnosis of PD and accelerated the development of targeted therapies. Nevertheless, despite more than two decades of research, the cellular function, aggregation mechanisms, and induction of cellular damage by αSyn remain incompletely understood. Unraveling the interplay between αSyn, neurons, and glia may provide insights into disease initiation and progression, which may bring us closer to exploring new effective therapeutic strategies. Herein, we provide an overview of recent studies emphasizing the multifaceted nature of αSyn and its impact on both neuron and glial cell damage.

Indexed as

Neurodegenerative DiseasesParkinson Diseasealpha-SynucleinDopaminergic NeuronsNeurogliaalpha-Synucleinaggregationglial cellsLewy bodiesneurodegenerationneuroinflammationneuronsParkinson’s diseaseseedingα-synuclein

Identifiers

PMID38203531
PMCPMC10778752
OpenAlexW4390269548

What OpenQuestion holds

Textmetadata
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.