Mitochondria Dysfunction and Neuroinflammation in Neurodegeneration: Who Comes First?

Antioxidants, Journal Year: 2024, Volume and Issue: 13(2), P. 240 - 240

Published: Feb. 16, 2024

Neurodegenerative diseases (NDs) encompass an assorted array of disorders such as Alzheimer's disease, Parkinson's and amyotrophic lateral sclerosis, each characterised by distinct clinical manifestations underlying pathological mechanisms. While some cases have a genetic basis, many NDs occur sporadically. Despite their differences, these commonly feature chronic neuroinflammation hallmark. Consensus has recently been reached on the possibility that mitochondria dysfunction protein aggregation can mutually contribute to activation neuroinflammatory response thus onset progression disorders. In present review, we discuss contribution aetiology NDs, highlighting new potential therapeutic targets be identified tackle neurodegenerative processes alleviate pathologies.

Language: Английский

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Exploring the intricacies of calcium dysregulation in ischemic stroke: Insights into neuronal cell death and therapeutic strategies

Life Sciences, Journal Year: 2024, Volume and Issue: 347, P. 122651 - 122651

Published: April 19, 2024

Language: Английский

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Mitochondrial fission and fusion in neurodegenerative diseases:Ca2+ signalling

Molecular and Cellular Neuroscience, Journal Year: 2025, Volume and Issue: unknown, P. 103992 - 103992

Published: Jan. 1, 2025

Language: Английский

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The Brain Region Specific Citrullinome and PAD 1-6 Isozyme Detection in a Pre-motor Parkinson’s Disease Rat Model

Published: June 28, 2024

The detection of early biomarkers and molecular mechanisms in Parkinson’s disease (PD) remains a challenge. Recent research has pointed to potential roles for peptidylarginine deiminases (PADs), family calcium activated enzymes, associated post-translational protein citrul-lination/deimination stages the disease, with focus on hippocampal cortex re-gions brain. Further analysis brain region specific changes PAD isozymes identi-fication brain-region citrullinomes, therefore remain be studied. This study assessed isozyme expression (PADs 1-4; PAD6) citrullinated targets 6-hydroxydopamine (6-OHDA) induced rat model pre-motor PD. Cortex, hippocampus, striatum, midbrain, cerebellum olfactory bulb were compared between con-trols/shams PD model. In cortex, significant increase PAD2 PAD3 was observed PAD3, PAD4 PAD6 showed strongest levels, but no controls. reduction all bulb, significantly el-evated PAD2, signal signifi-cant cerebellum, seen Citrullinated hits most abundant while an particularly For regions there considerable difference IDs Citrullinome as-sociated KEGG pathways differed six regions; some overlapping controls PD, identified only, control brains only. onlywere: “Axon guidance”; “Spinocerebellar ataxia”; “Hippo signalling pathway”; “NOD-like receptor “Phosphatidyl-inositol system”; “Rap1 “Platelet activation”; “Yersinia infection”; “Fc gamma R-mediated phagocytosis”; “Human cytomegalovirus “Inositol phosphate metabolism”; “Thyroid hormone “Progesterone-mediated oocyte matura-tion”; “Oocyte meiosis”; “Choline metabolism cancer”. Our findings highlight differences isozymes, proteins regions,

Language: Английский

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Brain-Region-Specific Differences in Protein Citrullination/Deimination in a Pre-Motor Parkinson’s Disease Rat Model

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(20), P. 11168 - 11168

Published: Oct. 17, 2024

The detection of early molecular mechanisms and potential biomarkers in Parkinson’s disease (PD) remains a challenge. Recent research has pointed to novel roles for post-translational citrullination/deimination caused by peptidylarginine deiminases (PADs), family calcium-activated enzymes, the stages disease. current study assessed brain-region-specific citrullinated protein targets their associated protein–protein interaction networks alongside PAD isozymes 6-hydroxydopamine (6-OHDA) induced rat model pre-motor PD. Six brain regions (cortex, hippocampus, striatum, midbrain, cerebellum olfactory bulb) were compared between controls/shams PD model. For all regions, there was significant difference IDs controls. Citrullinated hits most abundant cortex followed cerebellum, bulb striatum. Citrullinome-associated pathway enrichment analysis showed correspondingly considerable differences six regions; some overlapping controls PD, identified only, control brains only. KEGG (Kyoto Encyclopedia Genes Genomes) pathways only with neurological, metabolic, immune hormonal functions included following: “Axon guidance”; “Spinocerebellar ataxia”; “Hippo signalling pathway”; “NOD-like receptor “Phosphatidylinositol system”; “Rap1 “Platelet activation”; “Yersinia infection”; “Fc gamma R-mediated phagocytosis”; “Human cytomegalovirus “Inositol phosphate metabolism”; “Thyroid hormone “Progesterone-mediated oocyte maturation”; “Oocyte meiosis”; “Choline metabolism cancer”. Some furthermore observed five (PADs 1, 2, 3, 4 6), changes 3 when comparing regions. Our findings indicate that PAD-mediated citrullination plays immune, cell neurodegenerative disease-related across highlighting PADs as future therapeutic avenues.

Language: Английский

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Calcium bridges built by mitochondria-associated endoplasmic reticulum membranes: potential targets for neural repair in neurological diseases

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(12), P. 3349 - 3369

Published: Nov. 13, 2024

The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions metabolic levels. Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels the membrane mitochondrial outer membrane, formed by various proteins protein complexes. This microstructural domain mediates several specialized functions, including calcium (Ca 2+ ) signaling, autophagy, morphology, oxidative stress response, apoptosis. Notably, dysregulation Ca signaling mediated mitochondria-associated is critical factor pathogenesis neurological diseases. Certain or complexes within these directly indirectly regulate distance mitochondria, well transduction signaling. Conversely, influences other membrane-associated functions. These can vary significantly across different diseases—such ischemic stroke, traumatic brain injury, Alzheimer’s disease, Parkinson’s amyotrophic lateral sclerosis, Huntington’s disease—and their respective stages progression. Targeted modulation disease-related pathways functional enhance function promote regeneration repair damaged neurons. Therefore, membranes-mediated pivotal pathological progression diseases represents significant potential therapeutic target. review focuses on effects distinct roles diseases, specifically highlighting early protective neuronal damage that result from prolonged overload deficiency. article provides comprehensive analysis mechanisms contributing to exploration targets for promoting neuroprotection nerve repair.

Language: Английский

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Modalities of cell death, survival and adaptation: The role of the Ca2+-signaling toolkit

Cell Calcium, Journal Year: 2023, Volume and Issue: 115, P. 102795 - 102795

Published: Aug. 28, 2023

Language: Английский

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