Evidence map›Paper›PMID 37725330›Full record

ArticlePharmacological reports : PR2023

Investigating the potential effects of α-synuclein aggregation on susceptibility to chronic stress in a mouse Parkinson's disease model.

Anna Alwani, Katarzyna Maziarz, Gabriela Burda, Monika Jankowska-Kiełtyka, Adam Roman, Gabriela Łyszczarz, Safak Er, Justyna Barut, Olga Barczyk-Woźnicka, Elżbieta Pyza and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Pharmacological reports : PR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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

13 authors at 3 institutions in 2 countries.

Anna AlwaniDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0002-7611-5467
Katarzyna MaziarzDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0001-9116-7954
Gabriela BurdaDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0001-6245-1606
Monika Jankowska-KiełtykaDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.
Adam RomanDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0003-0197-2453
Gabriela ŁyszczarzDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0003-3372-4155
Safak ErFaculty of Pharmacy, Drug Research Program, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0002-6752-0655
Justyna BarutDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0001-7314-381X
Olga Barczyk-WoźnickaDepartment of Cell Biology and Imaging, Institute of Zoology and Biomedical Research, Jagiellonian University, Gronostajowa 9, 30-387, Kraków, Poland.ORCID http://orcid.org/0000-0002-7500-5047
Elżbieta PyzaDepartment of Cell Biology and Imaging, Institute of Zoology and Biomedical Research, Jagiellonian University, Gronostajowa 9, 30-387, Kraków, Poland.ORCID http://orcid.org/0000-0003-1503-9533
Grzegorz KreinerDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0003-3719-2889
Irena NalepaDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland.ORCID http://orcid.org/0000-0002-7821-0206
Piotr ChmielarzDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343, Kraków, Poland. chmiel@if-pan.krakow.pl.ORCID http://orcid.org/0000-0001-8935-8591
Maj Institute of Pharmacology · PLJagiellonian University · PLUniversity of Helsinki · FI

Funding

Academy of Finland #293392Academy of Finland #319195Narodowe Centrum Nauki 2018/02/X/NZ4/02712
6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is a motor disorder characterized by the degeneration of dopaminergic neurons, putatively due to the accumulation of α-synuclein (α-syn) in Lewy bodies (LBs) in Substantia Nigra. PD is also associated with the formation of LBs in brain areas responsible for emotional and cognitive regulation such as the amygdala and prefrontal cortex, and concurrent depression prevalence in PD patients. The exact link between dopaminergic cell loss, α-syn aggregation, depression, and stress, a major depression risk factor, is unclear. Therefore, we aimed to explore the interplay between sensitivity to chronic stress and α-syn aggregation.

methodsBilateral injections of α-syn preformed fibrils (PFFs) into the striatum of C57Bl/6 J mice were used to induce α-syn aggregation. Three months after injections, animals were exposed to chronic social defeat stress.

resultsα-syn aggregation did not affect stress susceptibility but independently caused increased locomotor activity in the open field test, reduced anxiety in the light-dark box test, and increased active time in the tail suspension test. Ex vivo analysis revealed modest dopaminergic neuron loss in the substantia nigra and reduced dopaminergic innervation in the dorsal striatum in PFFs injected groups. α-Syn aggregates were prominent in the amygdala, prefrontal cortex, and substantia nigra, with minimal α-syn aggregation in the raphe nuclei and locus coeruleus.

conclusionsProgressive bilateral α-syn aggregation might lead to compensatory activity increase and alterations in emotionally regulated behavior, without affecting stress susceptibility. Understanding how α-syn aggregation and degeneration in specific brain structures contribute to depression and anxiety in PD patients requires further investigation.

Indexed as

Parkinson Diseasealpha-SynucleinAnimalsBrainCorpus StriatumDopaminergic NeuronsHumansMiceSubstantia Nigraalpha-SynucleinSnca protein, mouseChronic stressDepressionNon-motor symptomsParkinson’s diseasePreformed fibrilsα-synuclein

Identifiers

PMID37725330
PMCPMC10661792
OpenAlexW4386852188

What OpenQuestion holds

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Registered trials

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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.