Publications by authors named "Tong-Yao Gao"
Article Synopsis
- - Nicotinamide phosphoribosyltransferase (NAMPT) is vital for producing nicotinamide adenine dinucleotide (NAD) and has been studied for its protective effects in neurodegeneration, particularly in Alzheimer's Disease, but its role in Parkinson's Disease (PD) is less understood.
- - Research indicates that dopaminergic neurons in the substantia nigra have higher NAMPT levels, and removing NAMPT leads to the loss of these neurons, dopamine pathway impairment, and symptoms similar to PD in mice.
- - The study suggests that NAD precursor nicotinamide ribose (NR) can counteract neurodegeneration in PD by repairing dopamine pathways and highlights the potential for using NAD precursors in
Article Synopsis
- PARP-1 activity increases significantly during cerebral ischemia/reperfusion, leading to NAD deficiency and contributing to neuronal death.
- Activation of PARP-1 results in PARylation of key metabolic enzymes, hexokinase-1 and lactate dehydrogenase-B, disrupting energy metabolism in neurons.
- Inhibiting PARP-1 improves enzyme activity, reduces brain injury, and, when combined with pyruvate, shows promise as a therapeutic strategy for ischemic brain injury in mice.
Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme in the salvaging synthesis pathway of the nicotinamide adenine dinucleotide (NAD). Both NAMPT and NAD progressively decline upon aging and neurodegenerative diseases. The depletion of NAMPT induces mitochondrial dysfunction in motor neurons and causes bioenergetic stress in neurons.
View Article and Find Full Text PDFNicotinamide phosphoribosyltransferase inhibitor ameliorates mouse aging-induced cognitive impairment.
J Cereb Blood Flow Metab
October 2021
Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway. Though NAMPT inhibitors such as FK866 were originally developed as anti-cancer drugs, they also display neuroprotective effects. Here we show that the administration of FK866 at 0.
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