Evidence map›Paper›PMID 32788448›Full record

ArticleNeural regeneration research2021

Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process.

Mariana Toricelli, Arthur Antonio Ruiz Pereira, Guilherme Souza Abrao, Helena Nascimento Malerba, Julia Maia, Hudson Sousa Buck, Tania Araujo Viel

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 97 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Mariana ToricelliDepartment of Physiological Sciences, Santa Casa de Sao Paulo School of Medical Sciences, Sao Paulo, Brazil.
Arthur Antonio Ruiz PereiraLaboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil.
Guilherme Souza AbraoLaboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil.
Helena Nascimento MalerbaLaboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil.
Julia MaiaLaboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil.
Hudson Sousa BuckDepartment of Physiological Sciences, Santa Casa de Sao Paulo School of Medical Sciences, Sao Paulo, Brazil.
Tania Araujo VielLaboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil.
Universidade de São Paulo · BRFaculdade de Ciências Médicas da Santa Casa de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual's vulnerability to various diseases. The growth in the number of aging populations has increased the prevalence of chronic degenerative diseases, impairment of the central nervous system and dementias, such as Alzheimer's disease, whose main risk factor is age, leading to an increase of the number of individuals who need daily support for life activities. Some theories about aging suggest it is caused by an increase of cellular senescence and reactive oxygen species, which leads to inflammation, oxidation, cell membrane damage and consequently neuronal death. Also, mitochondrial mutations, which are generated throughout the aging process, can lead to changes in energy production, deficiencies in electron transport and apoptosis induction that can result in decreased function. Additionally, increasing cellular senescence and the release of proinflammatory cytokines can cause irreversible damage to neuronal cells. Recent reports point to the importance of changing lifestyle by increasing physical exercise, improving nutrition and environmental enrichment to activate neuroprotective defense mechanisms. Therefore, this review aims to address the latest information about the different mechanisms related to neuroplasticity and neuronal death and to provide strategies that can improve neuroprotection and decrease the neurodegeneration caused by aging and environmental stressors.

Indexed as

cell senescencecell signalingcholinergicenriched environmentlong-term potentiationneurodegenerationneurogenesisneuroinflammatoryneuronal deathneuroprotectionneurotophin

Identifiers

PMID32788448
PMCPMC7818866
OpenAlexW3048379582

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.