Interactions of Cellular Energetic Gene Clusters in the Alzheimer’s Mouse Brain DOI
Raghavan Raju,

Lun Cai,

Alpna Tyagi

et al.

Molecular Neurobiology, Journal Year: 2023, Volume and Issue: unknown

Published: Aug. 26, 2023

Language: Английский

Mitochondria in Alzheimer’s Disease Pathogenesis DOI Creative Commons
Allison B. Reiss,

Shelly Gulkarov,

Benna Jacob

et al.

Life, Journal Year: 2024, Volume and Issue: 14(2), P. 196 - 196

Published: Jan. 30, 2024

Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder that primarily affects persons aged 65 years above. It causes dementia with memory loss deterioration in thinking language skills. AD characterized by specific pathology resulting from the accumulation brain of extracellular plaques amyloid-β intracellular tangles phosphorylated tau. The importance mitochondrial dysfunction pathogenesis, while previously underrecognized, now more appreciated. Mitochondria are an essential organelle involved cellular bioenergetics signaling pathways. Mitochondrial processes crucial for synaptic activity such as mitophagy, trafficking, fission, fusion dysregulated brain. Excess fission fragmentation yield mitochondria low energy production. Reduced glucose metabolism also observed hypometabolic state, particularly temporo-parietal regions. This review addresses multiple ways which abnormal structure function contribute to AD. Disruption electron transport chain ATP production neurotoxic because cells have disproportionately high demands. In addition, oxidative stress, extremely damaging nerve cells, rises dramatically dyshomeostasis. Restoring health may be viable approach treatment.

Language: Английский

Citations

28

Mitochondria in aging and age-associated diseases DOI Creative Commons
Sonu Pahal, Nirjal Mainali, Meenakshisundaram Balasubramaniam

et al.

Mitochondrion, Journal Year: 2025, Volume and Issue: 82, P. 102022 - 102022

Published: Feb. 27, 2025

Mitochondria, essential for cellular energy, are crucial in neurodegenerative disorders (NDDs) and their age-related progression. This review highlights mitochondrial dynamics, mitovesicles, homeostasis, organelle communication. We examine impacts from aging NDDs, focusing on protein aggregation dysfunction. Prospective therapeutic approaches include enhancing mitophagy, improving respiratory chain function, maintaining calcium lipid balance, using microRNAs, transfer to protect function. These strategies underscore the role of health neuronal survival cognitive functions, offering new opportunities.

Language: Английский

Citations

3

Perivascular macrophages in cerebrovascular diseases DOI Creative Commons
Hiroki Uchikawa, Ken Uekawa, Yu Hasegawa

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 374, P. 114680 - 114680

Published: Jan. 6, 2024

Language: Английский

Citations

6

Recent advancements in the understanding of the alterations in mitochondrial biogenesis in Alzheimer’s disease DOI
Shreya Singh, Rakesh Kumar Singh

Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)

Published: Jan. 29, 2025

Language: Английский

Citations

0

DRP1, fission and apoptosis DOI Creative Commons
Nan Wang,

X.J. Wang,

Beiwu Lan

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: April 7, 2025

Language: Английский

Citations

0

Editorial for a New Section: Nutrition and Neuro Sciences DOI Open Access
Lorena Perrone, William B. Grant

Nutrients, Journal Year: 2025, Volume and Issue: 17(9), P. 1399 - 1399

Published: April 22, 2025

In December 2024, Nutrients launched a new section entitled “Nutrition and Neuro Sciences”, with the scope of collecting review research articles analyzing impact nutrition on cognitive function brain physiology throughout life [...]

Language: Английский

Citations

0

Role of mitochondrial quality control in neurodegenerative disease progression DOI Creative Commons
Tingting Liu,

Weibo Sun,

Shao-mei Guo

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: May 20, 2025

Neurodegenerative diseases are a diverse group of neurological disorders, in which abnormal mitochondrial function is closely associated with their development and progression. This has generated significant research interest the field. The proper functioning mitochondria relies on dynamic regulation quality control system. Key processes such as biogenesis, mitophagy, dynamics (division/fusion) essential for maintaining this balance. These collectively govern homeostasis. Therefore, system plays critical role onset progression neurodegenerative diseases. article provides concise overview molecular mechanisms involved dynamics, explores interactions, summarizes current progress understanding context

Language: Английский

Citations

0

Developing theragnostics for Alzheimer's disease: Insights from cancer treatment DOI Creative Commons
Hyunju Lee, Hee-Jeong Choi,

Yoo Joo Jeong

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 269, P. 131925 - 131925

Published: April 28, 2024

The prevalence of Alzheimer's disease (AD) and its associated economic societal burdens are on the rise, but there no curative treatments for AD. Interestingly, this neurodegenerative shares several biological pathophysiological features with cancer, including cell-cycle dysregulation, angiogenesis, mitochondrial dysfunction, protein misfolding, DNA damage. However, genetic factors contributing to overlap in processes between cancer AD have not been actively studied. In review, we discuss shared AD, molecular targets anticancer drugs, therapeutic approaches. First, outline common Second, describe their targets, effects pathology. Finally, how protein–protein interactions (PPIs), receptor inhibition, immunotherapy, gene therapy can be exploited cure management both Collectively, review provides insights development theragnostics based drugs targets.

Language: Английский

Citations

2

Functional implications of NHR-210 enrichment in C. elegans cephalic sheath glia: insights into metabolic and mitochondrial disruptions in Parkinson's disease models DOI Creative Commons
Rohil Hameed,

Anam Naseer,

Ankit Saxena

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: May 1, 2024

Abstract Glial cells constitute nearly half of the mammalian nervous system's cellular composition. The glia in C. elegans perform majority tasks comparable to those conducted by their equivalents. cephalic sheath (CEPsh) glia, which are known be counterparts astrocytes, enriched with two nuclear hormone receptors (NHRs)—NHR-210 and NHR-231. This unique enrichment makes CEPsh these NHRs intriguing subjects study concerning neuronal health. We endeavored assess role neurodegenerative diseases related functional processes, using transgenic expressing human alpha-synuclein. employed RNAi-mediated silencing, followed behavioural, functional, metabolic profiling relation suppression NHR-210 231. Our findings revealed that depleting nhr-210 changes dopamine-associated behaviour mitochondrial function alpha synuclein-expressing strains NL5901 UA44, through a putative target, pgp-9 , transmembrane transporter. Considering alteration involvement transporter, we performed metabolomics via HR-MAS NMR spectroscopy. Remarkably, substantial modifications ATP, betaine, lactate, glycine levels were seen upon absence . also detected considerable pathways such as phenylalanine, tyrosine, tryptophan biosynthesis metabolism; glycine, serine, threonine well glyoxalate dicarboxylate metabolism. In conclusion, deficiency receptor alpha-synuclein strain results altered function, coupled alterations vital metabolite levels. These underline physiological importance glia. Graphical abstract

Language: Английский

Citations

2

Drp1 Promotes Macrophage M1 Polarization and Inflammatory Response in Autoimmune Myocarditis by Driving Mitochondrial Fission DOI
Lin Lin, Jin Wei,

Jiahong Xue

et al.

Journal of Cardiovascular Translational Research, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 10, 2024

Language: Английский

Citations

2