Evidence map›Paper›PMID 35962936›Full record

ReviewNeurochemical research2022

Modulation of Inflammatory Mediators and Microglial Activation Through Physical Exercise in Alzheimer's and Parkinson's Diseases.

Erin John Rieger de Almeida, Hélio Jungkenn Ibrahim, Maria Rosa Chitolina Schetinger, Cinthia Melazzo de Andrade, Andréia Machado Cardoso

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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  12. Mechanisms of comorbidity between Alzheimer's disease and pain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

5 authors at 2 institutions in 1 country.

Erin John Rieger de AlmeidaGraduate Program in Physical Education From Federal University of Santa Maria, Santa Maria, RS, Brazil.
Hélio Jungkenn IbrahimFederal University of Fronteira Sul, Fronteira Sul, SC, Brazil.
Maria Rosa Chitolina SchetingerDepartment of Biochemistry and Molecular Biology, UFSM, Santa Maria, RS, Brazil.
Cinthia Melazzo de AndradeDepartment of Small Animal Clinic, Center of Rural Sciences, Federal University of Santa Maria-RS, Room 121, Veterinary Hospital Building, Avenue Roraima No. 1000, Santa Maria, RS, 97105-900, Brazil.
Andréia Machado CardosoGraduate Program in Physical Education From Federal University of Santa Maria, Santa Maria, RS, Brazil. deiaa.mc@gmail.com.ORCID http://orcid.org/0000-0003-4243-8855
Universidade Federal de Santa Maria · BRUniversidade Federal da Fronteira Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is an inflammatory process in the central nervous system (CNS), in addition to being one of the main features of Alzheimer's disease (AD) and Parkinson's disease (PD). Microglia are known for their immune functions and have multiple reactive phenotypes related to the types of stages involving neurodegenerative diseases. Depending on the state of activation of microglia in the CNS, it can be neuroprotective or neurotoxic. In this context, AD is a neurodegenerative and neuroinflammatory disease characterized by the deposition of beta-amyloid plaques, formation of fibrillar tangles of tau protein, and loss of neurons due to neurotoxic activation of microglia. However, PD is characterized by the loss of dopaminergic neurons in the substantia nigra and accumulation of alpha-synuclein in the cortical regions, spinal cord, and brain stem, which occurs by microglial activation, contributing to the neuroinflammatory process. In this aspect, the activation of microglia in both pathologies triggers high levels of inflammatory markers, such as interleukins, and causes the neuroinflammatory process of the diseases. Thus, physical exercise is pointed out as neuroprotective, as it can act to strengthen neurogenesis and reduce the inflammatory process. Therefore, the present review addresses the neuroprotective effect of microglia after different types of physical exercise protocols and evaluates the activity and effects of inflammatory and anti-inflammatory parameters and mechanisms of AD and PD. This review will discuss the anti-inflammatory effects of physical exercise through microglia activation with neuroprotective activity and the role of pro-and anti-inflammatory cytokines in AD and PD.

Indexed as

Alzheimer DiseaseNeuroprotective AgentsParkinson Diseasealpha-SynucleinAnti-Inflammatory AgentsCytokinesDopaminergic NeuronsExerciseHumansInflammation MediatorsMicrogliatau Proteinsalpha-SynucleinAnti-Inflammatory AgentsCytokinesInflammation MediatorsNeuroprotective Agentstau ProteinsAlzheimer's diseaseAnti-inflammatoryCytokinesNeuroinflammationParkinson's diseasePhysical exercise

Identifiers

PMID35962936
OpenAlexW4291115759

What Socratic holds

Textmetadata
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 Socratic graph.