8 pathways = Prana, page-2

Here is one of the abstracts by Dr. Sinclair ( September 2018). It is talking about NAD+, a product of mitochondrion and how this production is getting down by age. No wonder why he is interested in PBT434 helping mitochondria to get rid of iron hampering the energy production. This is just an example of his interest (metabolic and cardiovascular diseases). Sinclair will broaden the scope of Prana also to other areas than neurodegeneration and I would think their 6 companies and disease models can start with PBT434 very soon when the deal is completed.

Circ Res. 2018 Sep 14;123(7):868-885. doi: 10.1161/CIRCRESAHA.118.312498.
Sirtuins and NAD⁺ in the Development and Treatment of Metabolic and Cardiovascular Diseases.

Kane AE¹, Sinclair DA^1,2.
Author information


Abstract

The sirtuin family of nicotinamide adenine dinucleotide-dependent deacylases (SIRT1-7) are thought to be responsible, in large part, for the cardiometabolic benefits of lean diets and exercise and when upregulated can delay key aspects of aging. SIRT1, for example, protects against a decline in vascular endothelial function, metabolic syndrome, ischemia-reperfusion injury, obesity, and cardiomyopathy, and SIRT3 is protective against dyslipidemia and ischemia-reperfusion injury. With increasing age, however, nicotinamide adenine dinucleotide levels and sirtuin activity steadily decrease, and the decline is further exacerbated by obesity and sedentary lifestyles. Activation of sirtuins or nicotinamide adenine dinucleotide repletion induces angiogenesis, insulin sensitivity, and other health benefits in a wide range of age-related cardiovascular and metabolic disease models. Human clinical trials testing agents that activate SIRT1 or boost nicotinamide adenine dinucleotide levels are in progress and show promise in their ability to improve the health of cardiovascular and metabolic disease patients.​