Evidence map›Paper›PMID 38591201›Full record

ReviewCurrent topics in medicinal chemistry2024

Alleviating Neurodegenerative Diseases Associated with Mitochondrial Defects by Therapeutic Biomolecules.

Tanmoy Roy, Swarupanjali Padhi, Rupa Mazumder, Chandana Majee, Saumya Das, Monika, Rashmi Mishra, Bhupinder Kapoor

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current topics in medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Journal of experimental pharmacology · 2026
    Article
  2. 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

8 authors.

Tanmoy RoyDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Swarupanjali PadhiDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Rupa MazumderDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Chandana MajeeDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Saumya DasDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
MonikaDepartment of Pharmaceutics, Noida Institute of Engineering and Technology, Pharmacy Institute, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Rashmi MishraDepartment of Biotechnology, Noida Institute of Engineering and Technology, Greater Noida, Gautam Buddha Nagar, Uttar Pradesh, 201306, India.
Bhupinder KapoorSchool of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases are emerging as a global health concern in the current scenario, and their association with mitochondrial defects has been a potential area of research. Mitochondria, one of the essential organelles of the cell, serve as the cell's powerhouse, producing energy and ensuring cellular health. Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, and Pelizaeus-Merzbacher disease have been found to be primarily triggered by mitochondrial malfunction. One of the key byproducts of mitochondrial respiration, reactive oxygen species, also contributes significantly to mitochondrial DNA mutations that eventually cause mitochondrial breakdown. This review paper comprehensively examines the potential of therapeutic biomolecules, specifically mitochondria-specific antioxidants, in mitigating the impact of mitochondrial defects on neurodegenerative diseases. It provides a detailed analysis of the mechanisms involved in mitochondrial dysfunction, the potential therapeutic targets of these biomolecules, and their structureactivity relationship information are also discussed in this review. Various research articles and publications were used extensively in compiling the data, and the structures of biomolecules were prepared using software such as ChemDraw and ChemSketch. Crucial elements triggering mitochondrial abnormalities were identified and a tabular compilation of bioactive antioxidant compounds along with their therapeutic targets, was presented. Mitochondria-specific antioxidant therapy is an innovative and promising strategy for the management of neurodegenerative diseases associated with mitochondrial defects. This review provides a thorough summary of the current state of research and promising avenues of research and development in this field, emphasizing the importance of further investigations and clinical trials to elucidate their therapeutic benefits.

Indexed as

AntioxidantsMitochondriaNeurodegenerative DiseasesAnimalsHumansReactive Oxygen SpeciesAntioxidantsReactive Oxygen SpeciesAntioxidant therapyMitochondrial malfunctionmtDNA mutationNeurodegenerative diseasesOxidative stressROSStructure-activity relationship.

Identifiers

PMID38591201

What OpenQuestion 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 OpenQuestion graph.