Translations:Vitamin B3/6/en: Difference between revisions

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Severe vitamin B<sub>3</sub> deficiency in the diet causes the disease [[pellagra]], characterized by [[diarrhea]], sun-sensitive [[dermatitis]] involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death.> Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression. The biochemical mechanisms for the observed deficiency-caused neurodegeneration are not well understood, but may rest on A) the requirement for [[nicotinamide adenine dinucleotide]] (NAD+) to suppress the creation of neurotoxic tryptophan metabolites; B) inhibition of mitochondrial ATP generation resulting in cell damage; C) activation of the [[poly (ADP-ribose) polymerase]] (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective [[brain-derived neurotrophic factor]] or its receptor [[tropomyosin receptor kinase B]]; or, E) changes to [[Gene expression|genome expression]] directly due to the niacin deficiency.
Severe vitamin B<sub>3</sub> deficiency in the diet causes the disease [[pellagra]], characterized by [[diarrhea]], sun-sensitive [[dermatitis]] involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death. Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression. The biochemical mechanisms for the observed deficiency-caused neurodegeneration are not well understood, but may rest on A) the requirement for [[nicotinamide adenine dinucleotide]] (NAD+) to suppress the creation of neurotoxic tryptophan metabolites; B) inhibition of mitochondrial ATP generation resulting in cell damage; C) activation of the [[poly (ADP-ribose) polymerase]] (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective [[brain-derived neurotrophic factor]] or its receptor [[tropomyosin receptor kinase B]]; or, E) changes to [[Gene expression|genome expression]] directly due to the niacin deficiency.

Latest revision as of 22:08, 20 February 2024

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Message definition (Vitamin B3)
Severe vitamin B<sub>3</sub> deficiency in the diet causes the disease [[pellagra]], characterized by [[diarrhea]], sun-sensitive [[dermatitis]] involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death. Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression. The biochemical mechanisms for the observed deficiency-caused neurodegeneration are not well understood, but may rest on A) the requirement for [[nicotinamide adenine dinucleotide]] (NAD+) to suppress the creation of neurotoxic tryptophan metabolites; B) inhibition of mitochondrial ATP generation resulting in cell damage; C) activation of the [[poly (ADP-ribose) polymerase]] (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective [[brain-derived neurotrophic factor]] or its receptor [[tropomyosin receptor kinase B]]; or, E) changes to [[Gene expression|genome expression]] directly due to the niacin deficiency.

Severe vitamin B3 deficiency in the diet causes the disease pellagra, characterized by diarrhea, sun-sensitive dermatitis involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death. Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression. The biochemical mechanisms for the observed deficiency-caused neurodegeneration are not well understood, but may rest on A) the requirement for nicotinamide adenine dinucleotide (NAD+) to suppress the creation of neurotoxic tryptophan metabolites; B) inhibition of mitochondrial ATP generation resulting in cell damage; C) activation of the poly (ADP-ribose) polymerase (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective brain-derived neurotrophic factor or its receptor tropomyosin receptor kinase B; or, E) changes to genome expression directly due to the niacin deficiency.

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