Cargando…

Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease

[Image: see text] Alzheimer’s disease (AD) is a very complicated and multifactorial neurological disorder having limited therapeutic interventions illustrated by the impairment in memory and cognitive function. Several lines of confirmation are stoutly connected with mitochondrial function perturbat...

Descripción completa

Detalles Bibliográficos
Autores principales: Khatoon, Rehana, Kaushik, Pooja, Parvez, Suhel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2022
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9202010/
https://www.ncbi.nlm.nih.gov/pubmed/35721948
http://dx.doi.org/10.1021/acsomega.1c05653
_version_ 1784728439539892224
author Khatoon, Rehana
Kaushik, Pooja
Parvez, Suhel
author_facet Khatoon, Rehana
Kaushik, Pooja
Parvez, Suhel
author_sort Khatoon, Rehana
collection PubMed
description [Image: see text] Alzheimer’s disease (AD) is a very complicated and multifactorial neurological disorder having limited therapeutic interventions illustrated by the impairment in memory and cognitive function. Several lines of confirmation are stoutly connected with mitochondrial function perturbation as a significant causative factor in AD, while the molecular mechanisms involved in AD pathogenesis are still poorly understood. Minocycline, a well-known antibiotic, has confirmed efficacy against mitochondrial defects and oxidative stress as a neuroprotective effect. In view of this property, we examined the remedial effect of minocycline on AD. To attain insight into the molecular machinery responsible for AD pathogenesis, we preferred the UAS/GAL4 scheme for the development of AD in flies that overexpress the Aβ42 protein in the brain of Drosophila. The warning signs like the declined lifespan, locomotion deficit and memory loss, impaired mitochondrial membrane potential, and increased caspase 3 expression with mitogen-associated protein kinases linked with AD pathogenesis were examined in the existence of minocycline. Minocycline halted the Aβ42-induced symptoms including behavioral changes and altered the mitochondrial membrane potential along with apoptotic factors’ protein expression (JNK/p-JNK and caspase 3). Thus, the current study could be functional to find out the role of minocycline in human Aβ42-overexpressed transgenic AD flies.
format Online
Article
Text
id pubmed-9202010
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher American Chemical Society
record_format MEDLINE/PubMed
spelling pubmed-92020102022-06-17 Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease Khatoon, Rehana Kaushik, Pooja Parvez, Suhel ACS Omega [Image: see text] Alzheimer’s disease (AD) is a very complicated and multifactorial neurological disorder having limited therapeutic interventions illustrated by the impairment in memory and cognitive function. Several lines of confirmation are stoutly connected with mitochondrial function perturbation as a significant causative factor in AD, while the molecular mechanisms involved in AD pathogenesis are still poorly understood. Minocycline, a well-known antibiotic, has confirmed efficacy against mitochondrial defects and oxidative stress as a neuroprotective effect. In view of this property, we examined the remedial effect of minocycline on AD. To attain insight into the molecular machinery responsible for AD pathogenesis, we preferred the UAS/GAL4 scheme for the development of AD in flies that overexpress the Aβ42 protein in the brain of Drosophila. The warning signs like the declined lifespan, locomotion deficit and memory loss, impaired mitochondrial membrane potential, and increased caspase 3 expression with mitogen-associated protein kinases linked with AD pathogenesis were examined in the existence of minocycline. Minocycline halted the Aβ42-induced symptoms including behavioral changes and altered the mitochondrial membrane potential along with apoptotic factors’ protein expression (JNK/p-JNK and caspase 3). Thus, the current study could be functional to find out the role of minocycline in human Aβ42-overexpressed transgenic AD flies. American Chemical Society 2022-06-01 /pmc/articles/PMC9202010/ /pubmed/35721948 http://dx.doi.org/10.1021/acsomega.1c05653 Text en © 2022 The Authors. Published by American Chemical Society https://creativecommons.org/licenses/by-nc-nd/4.0/Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works (https://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Khatoon, Rehana
Kaushik, Pooja
Parvez, Suhel
Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title_full Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title_fullStr Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title_full_unstemmed Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title_short Mitochondria-Related Apoptosis Regulation by Minocycline: A Study on a Transgenic Drosophila Model of Alzheimer’s Disease
title_sort mitochondria-related apoptosis regulation by minocycline: a study on a transgenic drosophila model of alzheimer’s disease
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9202010/
https://www.ncbi.nlm.nih.gov/pubmed/35721948
http://dx.doi.org/10.1021/acsomega.1c05653
work_keys_str_mv AT khatoonrehana mitochondriarelatedapoptosisregulationbyminocyclineastudyonatransgenicdrosophilamodelofalzheimersdisease
AT kaushikpooja mitochondriarelatedapoptosisregulationbyminocyclineastudyonatransgenicdrosophilamodelofalzheimersdisease
AT parvezsuhel mitochondriarelatedapoptosisregulationbyminocyclineastudyonatransgenicdrosophilamodelofalzheimersdisease