ArticleJournal of neuroinflammation2022
Nicotinamide reverses deficits in puberty-born neurons and cognitive function after maternal separation.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- A systematic review of the therapeutic potential of nicotinamide adenine dinucleotide precursors for cognitive diseases in preclinical rodent models.BMC neuroscience · 2025Pooled it
- TRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.Schizophrenia bulletin · 2026Article
- GuiLingJi ameliorates mild cognitive impairment by targeting unsaturated fatty acid metabolism to inhibit GPR120/NF-κB mediated neuroinflammation.Frontiers in pharmacology · 2026Article
- Neuroprotective efficacy of methanolic extract of propolis against early life stress-induced oxidative and inflammatory damage: Involvement of the Nrf2-Keap1 signaling pathway.IBRO neuroscience reports · 2025Article
- Innovative Approaches to NAFLD: Exploring the Role of Nicotinamide in Multicellular Microtissue Models of Liver Fibrosis.Journal of cellular and molecular medicine · 2025Article
- Cognitive impairment following maternal separation in rats mediated by the NADTranslational psychiatry · 2025Article
- Understanding Role of Maternal Separation in Depression, Anxiety,and Pain Behaviour: A Mini Review of Preclinical Research With Focus on Neuroinflammatory Pathways.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2025Review
- Protective effect and mechanism of lycium barbarum polysaccharide against UVB-induced skin photoaging.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024Article
- Therapeutic application of nicotinamide: As a potential target for inhibiting fibrotic scar formation following spinal cord injury.CNS neuroscience & therapeutics · 2024Article
- Model construction and drug therapy of primary ovarian insufficiency by ultrasound-guided injection.Stem cell research & therapy · 2024Article
- Fecal microbiota transplantation alleviates cognitive impairment by improving gut microbiome composition and barrier function in male rats of traumatic brain injury following gas explosion.Frontiers in microbiology · 2024Article
- Capsaicin alleviates neuronal apoptosis and schizophrenia-like behavioral abnormalities induced by early life stress.Schizophrenia (Heidelberg, Germany) · 2023Article
- Macrophage/Microglia Sirt3 Contributes to the Anti-inflammatory Effects of Resveratrol Against Experimental Intracerebral Hemorrhage in Mice.Cellular and molecular neurobiology · 2023Article
- Nicotinamide ameliorates mitochondria-related neuronal apoptosis and cognitive impairment via the NADSchizophrenia (Heidelberg, Germany) · 2023Article
- Long-term environmental enrichment overcomes depression, learning, and memory impairment in elderly CD-1 mice with maternal sleep deprivation exposure.Frontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundEarly life stress (ELS) is associated with the development of schizophrenia later in life. The hippocampus develops significantly during childhood and is extremely reactive to stress. In rodent models, ELS can induce neuroinflammation, hippocampal neuronal loss, and schizophrenia-like behavior. While nicotinamide (NAM) can inhibit microglial inflammation, it is unknown whether NAM treatment during adolescence reduces hippocampal neuronal loss and abnormal behaviors induced by ELS.
methodsTwenty-four hours of maternal separation (MS) of Wistar rat pups on post-natal day (PND)9 was used as an ELS. On PND35, animals received a single intraperitoneal injection of BrdU to label dividing neurons and were given NAM from PND35 to PND65. Behavioral testing was performed. Western blotting and immunofluorescence staining were used to detect nicotinamide adenine dinucleotide (NAD
resultsCompared with controls, only MS animals in the adult stage (PND56-65) but not the adolescent stage (PND31-40) exhibited pre-pulse inhibition deficits and cognitive impairments mimicking schizophrenia symptoms. MS decreased the survival and activity of puberty-born neurons and hippocampal NAD
conclusionsMS may lead to schizophrenia-like phenotypes and persistent hippocampal abnormalities. NAM may be a safe and effective treatment in adolescence to restore normal hippocampal function and prevent or ameliorate schizophrenia-like behavior.
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Registered trials
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