Evidence map›Paper›PMID 39682694›Full record

ReviewCells2024

Neuronal Cell Rearrangement During Aging: Antioxidant Compounds as a Potential Therapeutic Approach.

Erjola Bej, Patrizia Cesare, Michele d'Angelo, Anna Rita Volpe, Vanessa Castelli

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Mitochondria as a Therapeutic Target in Metabolic Disorders.Mini reviews in medicinal chemistry · 2026
    Review
  5. Review
  6. Review
  7. 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

5 authors.

Erjola BejDepartment of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.
Patrizia CesareDepartment of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.
Michele d'AngeloDepartment of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0002-3693-840X
Anna Rita VolpeDepartment of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0002-1217-6412
Vanessa CastelliDepartment of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.ORCID 0000-0002-7005-3218

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a natural process that leads to time-related changes and a decrease in cognitive abilities, executive functions, and attention. In neuronal aging, brain cells struggle to respond to oxidative stress. The structure, function, and survival of neurons can be mediated by different pathways that are sensitive to oxidative stress and age-related low-energy states. Mitochondrial impairment is one of the most noticeable signs of brain aging. Damaged mitochondria are thought to be one of the main causes that feed the inflammation related to aging. Also, protein turnover is involved in age-related impairments. The brain, due to its high oxygen usage, is particularly susceptible to oxidative damage. This review explores the mechanisms underlying neuronal cell rearrangement during aging, focusing on morphological changes that contribute to cognitive decline and increased susceptibility to neurodegenerative diseases. Potential therapeutic approaches are discussed, including the use of antioxidants (e.g., Vitamin C, Vitamin E, glutathione, carotenoids, quercetin, resveratrol, and curcumin) to mitigate oxidative damage, enhance mitochondrial function, and maintain protein homeostasis. This comprehensive overview aims to provide insights into the cellular and molecular processes of neuronal aging and highlight promising therapeutic avenues to counteract age-related neuronal deterioration.

Indexed as

AgingAntioxidantsNeuronsOxidative StressAnimalsHumansMitochondriaAntioxidantsantioxidantsbrainmitochondrial dysfunctionneurodegenerationorganellesoxidative damageROS

Identifiers

PMID39682694
PMCPMC11639796

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.