Evidence map›Paper›PMID 32050617›Full record

ReviewInternational journal of molecular sciences2020

BDNF as a Promising Therapeutic Agent in Parkinson's Disease.

Ewelina Palasz, Adrianna Wysocka, Anna Gasiorowska, Malgorzata Chalimoniuk, Wiktor Niewiadomski, Grazyna Niewiadomska

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05854524 (Exploring the Biological Basis for Exercise Neuroprotection in Parkinson's Disease), which is not on this map. Cited by 262 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
262citing papers in PubMed, 9 pooled it
28.4field-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.

NCT05854524 narecruitingnot on this mapstarted 2024, after this paper: background citation

Exploring the Biological Basis for Exercise Neuroprotection in Parkinson's Disease

TypeinterventionalSponsorUniversity of Nevada, Las VegasRan2024 to 2026Enrolled90ConditionsParkinson DiseaseArmsAerobic exercise
3 · Its place in the literature

Who cites it

262 citing papers in PubMed, 9 syntheses or guidelines pooled it, 481 citations in OpenAlex.

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202 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

6 authors at 3 institutions in 1 country.

Ewelina PalaszMossakowski Medical Research Centre Polish Academy of Sciences, 02-106 Warsaw, Poland.
Adrianna WysockaNencki Institute of Experimental Biology Polish Academy of Sciences, 02-093 Warsaw, Poland.ORCID 0000-0002-3672-0611
Anna GasiorowskaMossakowski Medical Research Centre Polish Academy of Sciences, 02-106 Warsaw, Poland.
Malgorzata ChalimoniukFaculty in Biala Podlaska, Jozef Pilsudski University of Physical Education in Warsaw, 21-500 Warszawa, Poland.ORCID 0000-0003-0361-8626
Wiktor NiewiadomskiMossakowski Medical Research Centre Polish Academy of Sciences, 02-106 Warsaw, Poland.
Grazyna NiewiadomskaNencki Institute of Experimental Biology Polish Academy of Sciences, 02-093 Warsaw, Poland.
Mossakowski Medical Research Institute, Polish Academy of Sciences · PLInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLJózef Piłsudski University of Physical Education in Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) promotes neuroprotection and neuroregeneration. In animal models of Parkinson's disease (PD), BDNF enhances the survival of dopaminergic neurons, improves dopaminergic neurotransmission and motor performance. Pharmacological therapies of PD are symptom-targeting, and their effectiveness decreases with the progression of the disease; therefore, new therapeutical approaches are needed. Since, in both PD patients and animal PD models, decreased level of BDNF was found in the nigrostriatal pathway, it has been hypothesized that BDNF may serve as a therapeutic agent. Direct delivery of exogenous BDNF into the patient's brain did not relieve the symptoms of disease, nor did attempts to enhance BDNF expression with gene therapy. Physical training was neuroprotective in animal models of PD. This effect is mediated, at least partly, by BDNF. Animal studies revealed that physical activity increases BDNF and tropomyosin receptor kinase B (TrkB) expression, leading to inhibition of neurodegeneration through induction of transcription factors and expression of genes related to neuronal proliferation, survival, and inflammatory response. This review focuses on the evidence that increasing BDNF level due to gene modulation or physical exercise has a neuroprotective effect and could be considered as adjunctive therapy in PD.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorHumansNeuroprotective AgentsParkinson DiseaseBrain-Derived Neurotrophic FactorNeuroprotective Agentsbrain-derived neurotrophic factorneurodegenerationneuroprotectionParkinson’s diseasePD therapyphysical exercise

Identifiers

PMID32050617
PMCPMC7037114
OpenAlexW3004443958

What OpenQuestion holds

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Read underepoch 390

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.