Evidence map›Paper›PMID 36942213›Full record

ReviewHeliyon2023

Mitochondrial dysfunction: A notable contributor to the progression of Alzheimer's and Parkinson's disease.

Abolaji Samson Olagunju, Foysal Ahammad, Abiola Adeyanju Alagbe, Titilayomi Ayomide Otenaike, John Oluwafemi Teibo, Farhan Mohammad, Ahad Amer Alsaiari, Olabode Omotoso, Md Enamul Kabir Talukder

Open access · goldFull text readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

9 authors at 6 institutions in 4 countries.

Abolaji Samson OlagunjuDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Brazil.
Foysal AhammadDivision of Biological and Biomedical Sciences, College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.
Abiola Adeyanju AlagbeDepartment of Human Anatomy, University of Port Harcourt, Nigeria.
Titilayomi Ayomide OtenaikeDepartment of Genetics and Molecular Biology, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil.
John Oluwafemi TeiboDepartment of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP-Brazil, Av Bandeirantes, 3900, 14049- 900, Ribeirão Preto, SP, Brazil.
Farhan MohammadDivision of Biological and Biomedical Sciences, College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.
Ahad Amer AlsaiariDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif, Saudi Arabia.
Olabode OmotosoDepartment of Biochemistry, College of Medicine, University of Ibadan, Nigeria.
Md Enamul Kabir TalukderDepartment of Genetic Engineering and Biotechnology, Jashore University of Science and Technology, Jashore, Bangladesh.
Hamad bin Khalifa University · QAUniversidade de São Paulo · BRTaif University · SAUniversidade Federal do Rio Grande · BRUniversity of Ibadan · NGUniversity of Port Harcourt · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction remains a pivotal mechanism in manifold neurodegenerative diseases. Mitochondrial homeostasis within the cell is an essential aspect of cell biology. Mitochondria, the power-generating organelle of the cell, have a dominant role in several processes associated with genomic integrity and cellular equilibrium. They are involved in maintaining optimal cell functioning and ensuring guidance against possible DNA damage, which could lead to mutations and the onset of diseases. Conversely, system perturbations, which could be due to environmental factors or senescence, induce changes in the physiological balance and result in mitochondrial function impairment. As a result, we present a general overview of the pathological pathways involved in Alzheimer's and Parkinson's diseases caused by changes in mitochondrial homeostasis. The focal point of this review is on mitochondrial dysfunction being a significant condition in the onset of neuronal disintegration. We explain the pathways associated with the dysfunction of the mitochondria, which are common among the most recurring neurodegenerative diseases, including Alzheimer's and Parkinson's disease. Are mitochondrial dysfunctions an early event in the progression of neuropathological processes? We discovered that mtDNA mutation is a major contributor to the metabolic pathology of most neurological disorders, causing changes in genes important for physiological homeostasis. As a result, genetic changes in presenilin, Amyloid-, ABAD, DJ-1, PINK-1, PARKIN, alpha-synuclein, and other important controlling genes occur. Therefore, we suggest possible therapeutic solutions.

Indexed as

Alzheimer's diseaseAmyloid βMitochondrial dysfunctionNeurodegenerationParkinParkinson's disease

Identifiers

PMID36942213
PMCPMC10024096
OpenAlexW4323816831

What Socratic holds

Textfull text, public
LicenceCC BY
identifiers read3
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.