Pharmacologic rescue of motor and sensory function by the neuroprotective compound P7C3 following neonatal nerve injury

Early Detection of Subclinical Visual Damage After Blast-Mediated TBI Enables Prevention of Chronic Visual Deficit by Treatment With P7C3-S243

“…13 The vast majority of newborn hippocampal neurons die before structurally and functionally integrating into hippocampal circuitry, and the original P7C3 molecule was identified as an aminopropyl carbazole that blocked death of newborn hippocampal neurons without altering their rate of proliferation. [13][14][15][16] The P7C3 compounds also potently block cell death of mature neurons located in other regions of the central and peripheral nervous system, as shown through testing in animal models of stress-associated depression, 17 Parkinson's disease, 15,18 amyotrophic lateral sclerosis, 19 peripheral nerve crush injury, 20 and TBI. 9,21 In all of these cases, protection of neurons from cell death by P7C3 compounds correlated with preserved neurological function.…”

Mitochondrion as a Target for Heart Failure Therapy – Role of Protein Lysine Acetylation –

“…The process is affected by the cellular level of acetyl-CoA and/or the activity of acetyltransferases. Detailed information on the enzymes and substrates involved in protein LysAc is summarized in Table. [69][70][71][72][73][74][75][76][77][78][79][80][81][82][83] While the presence of histone acetyltransferases (HAT) in the nucleus is well established, the mode of acetyl group transfer for non-histone proteins is complex. tricarboxylic acid (TCA) cycle and produces the reducing equivalents NADH/FADH2.…”

Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice

“…This form of injury and its associated behavioral deficits can be recapitulated in rodent models, which may therefore be useful for discovery and validation of new therapeutic approaches (Goldstein et al, 2012; Mohan et al, 2013; Yin et al, 2014). Pharmcologic agents shown to enhance flux of the nicotinamide adenine dinucleotide (NAD) salvage pathway in normal mammalian cells and facilitate NAD rebound following doxorubicin exposure (Pieper et al, 2010, 2014; MacMillan et al, 2011; Wang et al, 2014) confer protective efficacy on pathology and behavior in a rodent model of blast-mediated TBI (Yin et al, 2014), as well as other models of neurodegeneration in the central and peripheral nervous systems (De Jesús-Cortés et al, 2012, 2015,2016; Tesla et al, 2012; Blaya et al, 2014; Dutca et al, 2014; Naidoo et al, 2014; Kemp et al, 2015; Walker et al, 2015; Lee et al, 2016). In addition, treatment with NAD and NAD precursors, including nicotinamide, nicotonic acid mononucleotide, and nicotinamide mononucleotide (NMN), or overexpression of nicotinamide phosphoribosyltransferase protect axons in vitro (Araki et al, 2004; Wang et al, 2005; Sasaki et al, 2006).…”