The neuroprotective compound P7C3-A20 promotes neurogenesis and improves cognitive function after ischemic stroke

How many decades will it take before followup studies are done in humans? I'm guessing never because we have fucking failures of stroke associations and NO stroke strategy or stroke leadership. Or you just could hire your own researchers to test this out.
http://www.sciencedirect.com/science/article/pii/S0014488617300055

• Zachary B. Loris^{a, b},
• Andrew A. Pieper^{c, ,} ,
• W. Dalton Dietrich^{a, b, ,}

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http://dx.doi.org/10.1016/j.expneurol.2017.01.006

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Highlights

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The neuroprotective compound P7C3-A20 was proposed as a therapeutic for stroke.

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P7C3-A20 reduced sensorimotor and cognitive deficits that occur after stroke.

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P7C3-A20 significantly increased neurogenesis in both neurogenic niches.

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P7C3-A20 significantly reduced both hippocampal and cortical atrophy which was strongly correlated to tissue sparing.

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P7C3-A20 treatment enhanced flux of nicotinamide adenine dinucleotide.

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Abstract

Ischemic stroke is a devastating condition with few therapeutic interventions available. The neuroprotective compound P7C3-A20 inhibits mature neuronal cell death while also increasing the net magnitude of postnatal neurogenesis in models of neurodegeneration and acute injury. P7C3 compounds enhance flux of nicotinamide adenine dinucleotide (NAD) in mammalian cells, a proposed therapeutic approach to treating cerebral ischemia. The effectiveness of P7C3-A20 treatment on chronic histopathological and behavioral outcomes and neurogenesis after ischemic stroke has not previously been established. Here, a transient middle cerebral artery occlusion in rats was followed by twice daily injection of P7C3-A20 or vehicle for 7 days. P7C3-A20-treated rats performed significantly better than vehicle-treated controls in sensorimotor cylinder and grid-walk tasks, and in a chronic test of spatial learning and memory. These behavioral improvements with P7C3-A20 treatment were correlated with significantly decreased cortical and hippocampal atrophy, and associated with increased neurogenesis in the subventricular zone and hippocampal dentate gyrus subgranular zone. Furthermore, cerebral ischemia significantly reduced NAD in the cortex but P7C3-A20 treatment restored NAD to sham levels. Thus, P7C3-A20 treatment mitigates neurodegeneration and augments repair in the brain after focal ischemia, which translates into chronic behavioral improvement. This suggests a new therapeutic approach of using P7C3 compounds to safely augment NAD and thereby promote two independent processes critical to protecting the brain from ischemic stroke: mature neuron survival and postnatal hippocampal neurogenesis throughout the post-ischemic brain.

Keywords

• Aminopropyl carbazole;
• Ischemic stroke;
• Neuroprotection;
• Neurogenesis;
• P7C3-A20;
• NAD

Correspondence to: Andrew A. Pieper, Department of Psychiatry, University of Iowa Carver College of Medicine, 200 Hawkins Ave, PBDB 1318, Iowa City, IA 52242, United States.

Correspondence to: W. Dalton Dietrich, Department of Neurological Surgery, University of Miami Leonard M. Miller School of Medicine, 1095 NW 14th Terrace, Suite 2-30, Miami, FL 33136-1060, United States.