Browsing by Author "Lopicic, Srdjan (8839362200)"

In the present review we have discussed the occurrence of β-N-methylamino-L-alanine (BMAA) and its natural isomers, and the organisms and sample types in which the toxin(s) have been detected. Further, the review discusses general pathogenic mechanisms of neurodegenerative diseases, and how modes of action of BMAA fit in those mechanisms. The biogeography of BMAA occurrence presented here contributes to the planning of epidemiological research based on the geographical distribution of BMAA and human exposure. Analysis of BMAA mechanisms in relation to pathogenic processes of neurodegeneration is used to critically assess the potential significance of the amino acid as well as to identify gaps in our understanding. Taken together, these two approaches provide the basis for the discussion on the potential role of BMAA as a secondary factor in neurodegenerative diseases, the rationale for further research and possible directions the research can take, which are outlined in the conclusions. © 2022 by the authors.

In the present review we have discussed the occurrence of β-N-methylamino-L-alanine (BMAA) and its natural isomers, and the organisms and sample types in which the toxin(s) have been detected. Further, the review discusses general pathogenic mechanisms of neurodegenerative diseases, and how modes of action of BMAA fit in those mechanisms. The biogeography of BMAA occurrence presented here contributes to the planning of epidemiological research based on the geographical distribution of BMAA and human exposure. Analysis of BMAA mechanisms in relation to pathogenic processes of neurodegeneration is used to critically assess the potential significance of the amino acid as well as to identify gaps in our understanding. Taken together, these two approaches provide the basis for the discussion on the potential role of BMAA as a secondary factor in neurodegenerative diseases, the rationale for further research and possible directions the research can take, which are outlined in the conclusions. © 2022 by the authors.

Neuromuscular excitability is a vital body function, and Mg2+ is an essential regulatory cation for the function of excitable membranes. Loss of Mg2+ homeostasis disturbs fluxes of other cations across cell membranes, leading to pathophysiological electrogenesis, which can eventually cause vital threat to the patient. Chronic subclinical Mg2+ deficiency is an increasingly prevalent condition in the general population. It is associated with an elevated risk of cardiovascular, respiratory and neurological conditions and an increased mortality. Magnesium favours bronchodilation (by antagonizing Ca2+ channels on airway smooth muscle and inhibiting the release of endogenous bronchoconstrictors). Magnesium exerts antihypertensive effects by reducing peripheral vascular resistance (increasing endothelial NO and PgI2 release and inhibiting Ca2+ influx into vascular smooth muscle). Magnesium deficiency disturbs heart impulse generation and propagation by prolonging cell depolarization (due to Na+/K+ pump and Kir channel dysfunction) and dysregulating cardiac gap junctions, causing arrhythmias, while prolonged diastolic Ca2+ release (through leaky RyRs) disturbs cardiac excitation-contraction coupling, compromising diastolic relaxation and systolic contraction. In the brain, Mg2+ regulates the function of ion channels and neurotransmitters (blocks voltage-gated Ca2+ channel-mediated transmitter release, antagonizes NMDARs, activates GABAARs, suppresses nAChR ion current and modulates gap junction channels) and blocks ACh release at neuromuscular junctions. Magnesium exerts multiple therapeutic neuroactive effects (antiepileptic, antimigraine, analgesic, neuroprotective, antidepressant, anxiolytic, etc.). This review focuses on the effects of Mg2+ on excitable tissues in health and disease. As a natural membrane stabilizer, Mg2+ opposes the development of many conditions of hyperexcitability. Its beneficial recompensation and supplementation help treat hyperexcitability and should therefore be considered wherever needed. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.

Neuromuscular excitability is a vital body function, and Mg2+ is an essential regulatory cation for the function of excitable membranes. Loss of Mg2+ homeostasis disturbs fluxes of other cations across cell membranes, leading to pathophysiological electrogenesis, which can eventually cause vital threat to the patient. Chronic subclinical Mg2+ deficiency is an increasingly prevalent condition in the general population. It is associated with an elevated risk of cardiovascular, respiratory and neurological conditions and an increased mortality. Magnesium favours bronchodilation (by antagonizing Ca2+ channels on airway smooth muscle and inhibiting the release of endogenous bronchoconstrictors). Magnesium exerts antihypertensive effects by reducing peripheral vascular resistance (increasing endothelial NO and PgI2 release and inhibiting Ca2+ influx into vascular smooth muscle). Magnesium deficiency disturbs heart impulse generation and propagation by prolonging cell depolarization (due to Na+/K+ pump and Kir channel dysfunction) and dysregulating cardiac gap junctions, causing arrhythmias, while prolonged diastolic Ca2+ release (through leaky RyRs) disturbs cardiac excitation-contraction coupling, compromising diastolic relaxation and systolic contraction. In the brain, Mg2+ regulates the function of ion channels and neurotransmitters (blocks voltage-gated Ca2+ channel-mediated transmitter release, antagonizes NMDARs, activates GABAARs, suppresses nAChR ion current and modulates gap junction channels) and blocks ACh release at neuromuscular junctions. Magnesium exerts multiple therapeutic neuroactive effects (antiepileptic, antimigraine, analgesic, neuroprotective, antidepressant, anxiolytic, etc.). This review focuses on the effects of Mg2+ on excitable tissues in health and disease. As a natural membrane stabilizer, Mg2+ opposes the development of many conditions of hyperexcitability. Its beneficial recompensation and supplementation help treat hyperexcitability and should therefore be considered wherever needed. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.