ArticleNeuroscience letters2015
Chronic P7C3 treatment restores hippocampal neurogenesis in the Ts65Dn mouse model of Down Syndrome [Corrected].
Article in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome.Brain research bulletin · 2026Article
- Targeting NAD Metabolism for the Therapy of Age-Related Neurodegenerative Diseases.Neuroscience bulletin · 2024Review
- Review
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Cardioprotective Effects of 1-(3,6-Dibromo-carbazol-9-yl)-3-Phenylamino-Propan-2-Ol in Diabetic Hearts via Nicotinamide Phosphoribosyltransferase Activation.The Journal of pharmacology and experimental therapeutics · 2022Article
- Prenatal and Postnatal Pharmacotherapy in Down Syndrome: The Search to Prevent or Ameliorate Neurodevelopmental and Neurodegenerative Disorders.Annual review of pharmacology and toxicology · 2022Article
- The flavonoid 7,8-DHF fosters prenatal brain proliferation potency in a mouse model of Down syndrome.Scientific reports · 2021Article
- The Antipsychotic D2AAK1 as a Memory Enhancer for Treatment of Mental and Neurodegenerative Diseases.International journal of molecular sciences · 2020Article
- Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures.Hippocampus · 2019Article
- Selective Nonnuclear Estrogen Receptor Activation Decreases Stroke Severity and Promotes Functional Recovery in Female Mice.Endocrinology · 2018Article
- Rodent models in Down syndrome research: impact and future opportunities.Disease models & mechanisms · 2017Review
- The medial temporal memory system in Down syndrome: Translating animal models of hippocampal compromise.Hippocampus · 2017Article
- Recent Advances in Neurogenic Small Molecules as Innovative Treatments for Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2016Review
- Neuroprotective Efficacy of an Aminopropyl Carbazole Derivative P7C3-A20 in Ischemic Stroke.CNS neuroscience & therapeutics · 2016Article
- Targeting Nicotinamide Phosphoribosyltransferase as a Potential Therapeutic Strategy to Restore Adult Neurogenesis.CNS neuroscience & therapeutics · 2016Review
- Timing of therapies for Down syndrome: the sooner, the better.Frontiers in behavioral neuroscience · 2015Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Down syndrome (DS) is the most common genetic cause of intellectual disability and developmental delay. In addition to cognitive dysfunction, DS patients are marked by diminished neurogenesis, a neuropathological feature also found in the Ts65Dn mouse model of DS. Interestingly, manipulations that enhance neurogenesis - like environmental enrichment or pharmacological agents - improve cognition in Ts65Dn mice. P7C3 is a proneurogenic compound that enhances hippocampal neurogenesis, cell survival, and promotes cognition in aged animals. However, this compound has not been tested in the Ts65Dn mouse model of DS. We hypothesized that P7C3 treatment would reverse or ameliorate the neurogenic deficits in Ts65Dn mice. To test this, adult Ts65Dn and age-matched wild-type (WT) mice were administered vehicle or P7C3 twice daily for 3 months. After 3 months, brains were examined for indices of neurogenesis, including quantification of Ki67, DCX, activated caspase-3 (AC3), and surviving BrdU-immunoreactive(+) cells in the granule cell layer (GCL) of the hippocampal dentate gyrus. P7C3 had no effect on total Ki67+, DCX+, AC3+, or surviving BrdU+ cells in WT mice relative to vehicle. GCL volume was also not changed. In keeping with our hypothesis, however, P7C3-treated Ts65Dn mice had a significant increase in total Ki67+, DCX+, and surviving BrdU+ cells relative to vehicle. P7C3 treatment also decreased AC3+ cell number but had no effect on total GCL volume in Ts65Dn mice. Our findings show 3 months of P7C3 is sufficient to restore the neurogenic deficits observed in the Ts65Dn mouse model of DS.
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