Difference between revisions of "Selenium"
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== Effects on ALS == | == Effects on ALS == | ||
| − | "Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. '''Selenium is vital for the brain and seems to participate in the pathology of disorders such as''' Alzheimer's disease, Parkinson's disease, '''amyotrophic lateral sclerosis''' and epilepsy. Since selenium was '''shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed'''. The aim of the present review is to analyse possible relations between selenium and neurotransmission. '''Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus'''. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. '''The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2)'''." | + | "Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. '''Selenium is vital for the brain and seems to participate in the pathology of disorders such as''' Alzheimer's disease, Parkinson's disease, '''amyotrophic lateral sclerosis''' and epilepsy. Since selenium was '''shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed'''. The aim of the present review is to analyse possible relations between selenium and neurotransmission. '''Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus'''. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. '''The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2)'''."{{#pmid:26398431|solovyev2015}} |
=== Regulated pathways === | === Regulated pathways === | ||
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==Cautions and risks== | ==Cautions and risks== | ||
| + | Selenium is toxic in its inorganic hexavalent form (selenate) and increases ALS risk, among several other diseases.{{#pmid:27344266|vinceti2016}} | ||
== Discussion threads on the ALSTDI forum == | == Discussion threads on the ALSTDI forum == | ||
Revision as of 15:46, 29 July 2017
Information on nutritional supplements people with ALS have been taking
Contents
Effects on ALS
"Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. Selenium is vital for the brain and seems to participate in the pathology of disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and epilepsy. Since selenium was shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed. The aim of the present review is to analyse possible relations between selenium and neurotransmission. Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2)."[1]
Regulated pathways
Possible synergies
Cautions and risks
Selenium is toxic in its inorganic hexavalent form (selenate) and increases ALS risk, among several other diseases.[2]
Discussion threads on the ALSTDI forum
Where to get it
References
- ↑ Solovyev &: Importance of selenium and selenoprotein for brain function: From antioxidant protection to neuronal signalling. J. Inorg. Biochem. 2015;153:1-12. PMID: 26398431. DOI. Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. Selenium is vital for the brain and seems to participate in the pathology of disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and epilepsy. Since selenium was shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed. The aim of the present review is to analyse possible relations between selenium and neurotransmission. Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2).
- ↑ Vinceti et al.: Long-term mortality patterns in a residential cohort exposed to inorganic selenium in drinking water. Environ. Res. 2016;150:348-56. PMID: 27344266. DOI. Selenium (Se) is a metalloid of considerable nutritional and toxicological importance in humans. To date, limited epidemiologic evidence exists about the health effects of exposure to this trace element in drinking water. We investigated the relationship between Se levels in water and mortality in the municipality of Reggio Emilia, Italy, where high levels of Se were previously observed in drinking water. From 1974 to 1985, 2065 residents consumed drinking water with Se levels close to the European standard of 10μg/l, in its inorganic hexavalent form (selenate). Follow-up was conducted for the years 1986-2012 in Reggio Emilia and a lesser exposed comparison group of around 100,000 municipal residents, with comparable socio-demographic characteristics. Overall mortality from all causes, cardiovascular disease and cancer showed little evidence of differences. However, excess rate ratios were seen for some site specific cancers such as neoplasms of buccal cavity and pharynx, urinary tract, lymphohematopoietic tissue, melanoma, and two neurodegenerative diseases, Parkinson's disease and amyotrophic lateral sclerosis. Excess mortality in the exposed cohort for specific outcomes was concentrated in the first period of follow-up (1986-1997), and waned starting 10 years after the high exposure ended. We also found lower mortality from breast cancer in females during the first period of follow-up. When we extended the analysis to include residents who had been consuming the high-selenium drinking water for a shorter period, mortality rate ratios were also increased, but to a lesser extent. Overall, we found that the mortality patterns related to long-term exposure to inorganic hexavalent selenium through drinking water were elevated for several site-specific cancers and neurodegenerative disease.
