Unfortunately, this is not a free paper. In my opinion, ATH should give us a better version of this abstract because I think that this paper could tell us why Sinclair invested in ATH. So it could tell other potential investors that ATH is worth considering. Sinclair has published mostly vascular papers but now he is an author in a neurodegenerative paper, Prana´s old territory ( AD, PD, HD ). Of course, it may be better to wait until the "future PBT434 mitochondrion papers" are published ( hope soon) to make the connection between PBT434 and NAD+. The simple good news is that Sinclair has been writing this paper. It demonstrates that he is interested in neurodegeneration. But this is easy for him because he understands general cellular survival mechanisms and they are not so different in neural tissues. Old Prana was thinking that nerve tissues are different than others. They are, but not so much when we are dealing with energy supply and survival.Cell Metab. 2019 Oct 1;30(4):630-655. doi: 10.1016/j.cmet.2019.09.001.NAD+ in Brain Aging and Neurodegenerative Disorders.
Author information
- 1
- Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway.
- 2
- Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
- 3
- Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
- 4
- Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway; The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway. Electronic address: [email protected].
Abstract
NAD+ is a pivotal metabolite involved in cellular bioenergetics, genomic stability, mitochondrial homeostasis, adaptive stress responses, and cell survival. Multiple NAD+-dependent enzymes are involved in synaptic plasticity and neuronal stress resistance. Here, we review emerging findings that reveal key roles for NAD+ and related metabolites in the adaptation of neurons to a wide range of physiological stressors and in counteracting processes in neurodegenerative diseases, such as those occurring in Alzheimer's, Parkinson's, and Huntington diseases, and amyotrophic lateral sclerosis. Advances in understanding the molecular and cellular mechanisms of NAD+-based neuronal resilience will lead to novel approaches for facilitating healthy brain aging and for the treatment of a range of neurological disorders.
