Homocysteine: Neurotoxicity and mechanisms of induced hyperexcitability

Stanojlović, Olivera; Hrnčić, Dragan; Rašić-Marković, Aleksandra; Djurić, Dragan

doi:10.5937/sjecr1101003s

Cited by 2 publications

(2 citation statements)

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“…Several plausible mechanistic links have, however, been demonstrated, for example, hcy induction of neurotoxicity in animals. It is notable that neural tissue appears to be more sensitive to elevations in hcy than endothelial smooth muscle cells ( 198 ) , on which most research in this field has been focused. Relevant mechanisms in the CNS include: the inhibition of acetyl-cholinesterase activity (involved in neurotransmitter breakdown) in rats, N -methyl- d -aspartate (NMDA; glutamate) receptor interaction-induced excitotoxicity in neurons, and region-specific inhibition of Na + /K + -ATPase activity in the brain (resulting in inability to maintain cell polarity) ( 198 ) .…”

Section: Folate (Vitamin B9)mentioning

confidence: 99%

“…It is notable that neural tissue appears to be more sensitive to elevations in hcy than endothelial smooth muscle cells ( 198 ) , on which most research in this field has been focused. Relevant mechanisms in the CNS include: the inhibition of acetyl-cholinesterase activity (involved in neurotransmitter breakdown) in rats, N -methyl- d -aspartate (NMDA; glutamate) receptor interaction-induced excitotoxicity in neurons, and region-specific inhibition of Na + /K + -ATPase activity in the brain (resulting in inability to maintain cell polarity) ( 198 ) . In the PNS, hcy–NMDA receptor interaction has additionally been linked (in mice) to increased sensitivity to oxidative stress-induced inhibition of neurotransmitter release and associated loss of cell integrity at the level of the neuromuscular junction ( 199 ) , as in motorneurone disease.…”

Section: Folate (Vitamin B9)mentioning

confidence: 99%

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Selected B vitamins and their possible link to the aetiology of age-related sarcopenia: relevance of UK dietary recommendations

2018

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The possible roles of selected B vitamins in the development and progression of sarcopenia are reviewed. Age-related declines in muscle mass and function are associated with huge and increasing costs to healthcare providers. Falls and loss of mobility and independence due to declining muscle mass/function are associated with poor clinical outcomes and their prevention and management are attractive research targets. Nutritional status appears a key modifiable and affordable intervention. There is emerging evidence of sarcopenia being the result not only of diminished anabolic activity but also of declining neurological integrity in older age, which is emerging as an important aspect of the development of age-related decline in muscle mass/function. In this connection, several B vitamins can be viewed as not only cofactors in muscle synthetic processes, but also as neurotrophic agents with involvements in both bioenergetic and trophic pathways. The B vitamins thus selected are examined with respect to their relevance to multiple aspects of neuromuscular function and evidence is considered that requirements, intakes or absorption may be altered in the elderly. In addition, the evidence base for recommended intakes (UK recommended daily allowance) is examined with particular reference to original datasets and their relevance to older individuals. It is possible that inconsistencies in the literature with respect to the nutritional management of sarcopenia may, in part at least, be the result of compromised micronutrient status in some study participants. It is suggested that in order, for example, for intervention with amino acids to be successful, underlying micronutrient deficiencies must first be addressed/eliminated.

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Section: Folate (Vitamin B9)mentioning

confidence: 99%