Mitochondrial dysfunction and neurological disorders: A narrative review and treatment overview

Life Sciences, Journal Year: 2023, Volume and Issue: 334, P. 122257 - 122257

Published: Nov. 8, 2023

Language: Английский

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Oxidative stress and ion channels in neurodegenerative diseases

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Jan. 29, 2024

Numerous neurodegenerative diseases result from altered ion channel function and mutations. The intracellular redox status can significantly alter the gating characteristics of channels. Abundant associated with oxidative stress have been documented, including Parkinson’s, Alzheimer’s, spinocerebellar ataxia, amyotrophic lateral sclerosis, Huntington’s disease. Reactive oxygen nitrogen species compounds trigger posttranslational alterations that target specific sites within subunits responsible for assembly. These include adjustment cysteine residues through reactions induced by reactive (ROS), nitration, S-nitrosylation assisted nitric oxide tyrosine peroxynitrite. Several channels directly investigated their functional responses to oxidizing agents stress. This review primarily explores relationship potential links between in conditions, such as cerebellar ataxias Parkinson’s correlation could hold promise developing innovative therapies common diseases.

Language: Английский

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Calcium‐Dependent Signaling in Astrocytes: Downstream Mechanisms and Implications for Cognition

Journal of Neurochemistry, Journal Year: 2025, Volume and Issue: 169(2)

Published: Feb. 1, 2025

Astrocytes are glial cells recognized for their diverse roles in regulating brain circuit structure and function. They can sense adapt to changes the microenvironment due unique structural biochemical properties. A key aspect of astrocytic function involves calcium (Ca2+)-dependent signaling, which serves as a fundamental mechanism interactions with neurons other brain. However, while significant progress has been made understanding spatio-temporal properties Ca2+ signals, downstream molecular pathways exact mechanisms through astrocytes decode these signals regulate homeostatic physiological processes remain poorly understood. To address this topic, we review here available literature on sources intracellular Ca2+, well its signaling pathways. We well-studied Ca2+-dependent exocytosis but draw attention additional that less understood are, most likely, highly influential many cellular functions. Finally, how is thought underlie neuron-astrocyte regions involved cognitive processing.

Language: Английский

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Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer’s Disease and Vascular Dementia

Aging and Disease, Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 1, 2024

The blood-brain barrier (BBB) plays a critical role in maintaining ion and fluid homeostasis, essential for brain metabolism neuronal function. Regulation of nutrient, water, transport across the BBB is tightly controlled by specialized transporters channels located within its unique cellular components. These dynamic processes not only influence BBB’s structure but also impact vital signaling mechanisms, optimal Disruption ion, pH, balance at associated with pathology has been implicated various neurological conditions, including stroke, epilepsy, trauma, neurodegenerative diseases such as Alzheimer’s disease (AD). However, knowledge gaps exist regarding dysregulation on function dementias. Several factors contribute to this gap: complex nature these historical research focus mechanisms technical challenges studying in vivo models lack efficient vitro dementia models. This review provides an overview current roles poses specific questions: 1) How are expression activity key altered AD vascular (VaD); 2) Do changes dysfunction progression; 3) Can restoring mitigate improve clinical outcomes. Addressing will provide greater insight into disorders.

Language: Английский

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Small molecules targeting canonical transient receptor potential channels: an update

Drug Discovery Today, Journal Year: 2024, Volume and Issue: 29(5), P. 103951 - 103951

Published: March 20, 2024

Language: Английский

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Epigenetic Control of Hyperuricemia and Gout by Gene Writer DNMT1 and RNA Editor ADAR1: Mechanism of Gout and Amyloid Dissolution in Down Syndrome

Biochemical Genetics, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 29, 2025

Language: Английский

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Unscrambling the cellular and molecular threads of Neuroplasticity: Insights into Alzheimer’s disease pathogenesis

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

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Transcriptomic analysis of the TRP gene family in human brain physiopathology

Frontiers in Molecular Neuroscience, Journal Year: 2025, Volume and Issue: 18

Published: April 24, 2025

The transient receptor potential (TRP) gene family is vital to cellular physiology, mediating ion flow across membranes and facilitating sensory signal transduction. This article examines the transcriptomic landscape of TRP genes, emphasizing their varying expression organs, tissues, cells, with a particular focus on brain. Analysis reveals distinct spatial distribution expression, notably enriched in hippocampus during brain development, highlighting essential role neuronal function. Utilizing datasets from Human Protein Atlas, Allen Brain studies aging dementia, associations are identified between development or pathophysiology neural tissue, therapeutic channels addressing, e.g., impairments cognitive decline. These insights into regulatory dynamics lay foundation for developing targeted interventions neurodegenerative disorders.

Language: Английский

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Venom peptides regulating Ca2+ homeostasis: neuroprotective potential

Trends in Pharmacological Sciences, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

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A novel peptide inhibitor of TRPM2 channels improves recovery of memory function following traumatic brain injury

Frontiers in Synaptic Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: April 25, 2025

Traumatic Brain Injury (TBI) is a leading cause of mortality and morbidity in adults can lead to long-term disability, including cognitive motor deficits. Despite advances research, there are currently no pharmacological interventions improve outcomes after TBI. Studies suggest that non-selective transient receptor potential melastatin 2 (TRPM2) channels contribute brain injury models ischemia, however TRPM2 remains understudied following Thus, we utilized KO mice novel inhibiting peptide, tatM2NX, assess the role TBI-induced functional recovery. This study used histological analysis injury, neurobehavior electrophysiology on recovery (memory) impairments using controlled cortical impact (CCI) model induce TBI mice. Histological investigate volume at 7 days showed sex differences response but effects our WT A contextual fear-conditioning task was memory function or 30 demonstrates sham-operated exhibited significant freezing behavior compared TBI-operated mice, indicating impaired function. Mice administered tat-M2NX h reduction control tat-scrambled (tat-SCR)-treated suggesting improvement To test effect hippocampal potentiation (LTP), well-established cellular synaptic plasticity associated with changes learning memory, extracellular field recordings CA1 neurons were performed slices prepared Consistent behavioral testing, observed LTP (tat-SCR), sham However, treated preserved LTP, consistent improved studies. While this data implicates pathology TBI, without providing protection suggests administration tatM2NX an acute time point differentially affects regions regions.

Language: Английский

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