ArticleNPJ schizophrenia2019
MAP2 immunoreactivity deficit is conserved across the cerebral cortex within individuals with schizophrenia.
Article in NPJ schizophrenia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- Human Stem Cell-Derived Neurospheroids and a Multi-Assay Strategy Provide Brain Cytotoxicity New Insights from ADB-FUBIATA Exposure.Neurotoxicity research · 2026Article
- Review
- Maternal immune activation imprints translational dysregulation and differential MAP2 phosphorylation in descendant neural stem cells.Molecular psychiatry · 2025Article
- MAP2 phosphorylation: mechanisms, functional consequences, and emerging insights.Frontiers in cellular neuroscience · 2025Review
- Terminal type-specific cannabinoid CB1 receptor alterations in patients with schizophrenia: A pilot study.Neurobiology of disease · 2023Article
- Neuroprotection by Abdominal Ultrasound in Lipopolysaccharide-Induced Systemic Inflammation.International journal of molecular sciences · 2023Article
- Terminal type-specific cannabinoid CB1 receptor alterations in patients with schizophrenia: a pilot study.bioRxiv : the preprint server for biology · 2023Article
- More than a marker: potential pathogenic functions of MAP2.Frontiers in molecular neuroscience · 2022Article
- MAP2 is differentially phosphorylated in schizophrenia, altering its function.Molecular psychiatry · 2021Article
- Cardiac glycosaminoglycans and structural alterations during chronic stress-induced depression-like behavior in mice.American journal of physiology. Heart and circulatory physiology · 2021Article
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Several postmortem studies have reported lower levels of immunoreactivity (IR) for microtubule-associated protein 2 (MAP2) in several cortical regions of individuals with schizophrenia (SZ). However, whether this effect is conserved across multiple brain areas within an individual with SZ or if it is regionally-specific remains unclear. We characterized patterns of MAP2-IR across three cortical regions at different levels of the rostral-caudal axis within individual subjects with and without SZ. MAP2-IR levels were measured in deep layer 3 of dorsolateral prefrontal cortex (DLPFC), lateral intraparietal cortex (LIP), and primary visual cortex (V1). Postmortem tissue containing each cortical region was derived from 20 pairs of SZ subjects and nonpsychiatric comparison (NPC) subjects matched perfectly for sex, and as closely as possible for age and postmortem interval. MAP2-IR was assessed by quantitative fluorescence microscopy. We observed significantly lower levels of MAP2-IR in SZ subjects relative to NPC subjects, without a significant region by diagnosis interaction. Logs of the within-pair ratios (SZ:NPC) of MAP2-IR were significantly correlated across the three regions. These findings demonstrate that MAP2-IR deficits in SZ are consistent across three neocortical regions within individual subjects. This pattern of MAP2-IR deficit has implications for therapeutic development and future investigations of MAP2 pathology in SZ.
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Registered trials
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