Witamina B3 (nicotinamide, niagen, nicotinic acid)

Zaczęty przez niezaslepiony, 02 Maj 2017, 13:07:58

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Witam , mam artykuł , że witamina B3 a dokładnie jej formy pomagają w chorobach  neurodegeneracyjnych          

This is the main reason I take nicotinamide, Niagen and nicotinic acid (all types of vitamin B3). Overactivation of the enzyme called PARP-1 leads to rapid depletion of its substrate NAD. NAD depletion causes mitochondrial dysfunction and cell death. High dose B3 boosts NAD synthesis, thereby preventing neuronal cell death.

Semin Cell Dev Biol. 2016 Nov 17. pii: S1084-9521(16)30395-0. doi: 10.1016/j.semcdb.2016.11.007. [Epub ahead of print]
Poly(ADP-ribose)Polymerase-1 hyperactivation in neurodegenerative diseases: the death knell tolls for neurons.
Narne P1, Pandey V1, Simhadri PK1, Babu PP2.
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Abstract
Neurodegeneration is a salient feature of chronic refractory brain disorders like Alzheimer's, Parkinsons, Huntington's, amyotropic lateral sclerosis and acute conditions like cerebral ischemia/reperfusion etc. The pathological protein aggregates, mitochondrial mutations or ischemic insults typifying these disease conditions collude with and intensify existing oxidative stress and attendant mitochondrial dysfunction. Interlocking these mechanisms is poly(ADP-ribose) polymerase (PARP-1) hyperactivation that invokes a distinct form of neuronal cell death viz., 'parthanatos'. PARP-1, a typical 'moonlighting protein' by virtue of its ability to poly(ADP-ribosyl)ate a plethora of cellular proteins exerts diverse functions that impinge significantly on cellular processes. In addition, its interactions with various nuclear proteins like transcription factors and chromatin modifiers elicit varied transcriptional outcomes that wield pathological cellular responses. Further, emerging leitmotifs like mitochondrial and nucleolar PARPs and the novel aspects of gene expression regulation by PARP-1 and poly(ADP-ribosyl)ation can provide a holistic view of PARP-1's influence on cell vitality. In this review, we discuss the pathological underpinnings of PARP-1, with a special emphasis on mitochondrial dysfunction and cell death subroutines, in the realm of neurodegeneration. This would provide a deeper insight into the functions of PARP-1 in neurodegenerative conditions that would enable the development of more effective therapeutic strategies.

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