But one theory is that NAD-repletion would decrease oxidative stress and cell death. Hopefully that theory will be tested in animal studies, and if there are positive results, also in human studies.
Other molecules mentioned in this paper are: vitamin D, trehalose, tannins, and NAC. This paper has not been peer-reviewed.
https://www.preprints.org/manuscript/202003.0346/v1"NAD+ and niacin
In the depicted molecular pathology pathway of COVID-19, almost all procedures lead to or originate from NAD+ depletion. NAD+ depletion mediated by uncontrolled PARP activity leads to decreased sirtuin 1 (SIRT1) activity indirectly. SIRT1 deacetylates nuclear proteins using NAD+ to regulate the expression of genes including tumor suppressors, cytokines and proto-oncogenes and ultimately modulate inflammation, cell survival and apoptosis mechanisms.
NAD and ATP are prerequisite for each other and consumption of NAD in large amounts decreases ATP levels leading to impairment of all activities and integrity of the cell. In COVID-19-mediated ARDS, aldosterone level is decreased and patients are hypovolemic in spite of RAS activation. It seems that aldosterone synthesis is silenced somewhere in CNS or adrenal gland.
The logical interpretation is serotonin shortage which is an important molecule and has several roles in biology including stimulation of aldosterone secretion. In COVID-19 patients, the resources of tryptophan-as the raw material for serotonin and NAD synthesis in ARDS course of the disease serotonin is decreased and hypoaldostronism causes hyponatremia and hypovolemia.
Fatigue and various degrees of mood disorders are the consequences of NAD, ATP and serotonin reduction, which could be addressed by concomitant prescription of NAD, Niacin (Vitamin B3) and/or its precursor L-tryptophan with a PARP or PARG inhibitor.
It is possible that administration of NAD alone, along with high activity of PARP and PARG, worsen the clinical manifestation."