MAP2 immunoreactivity deficit is conserved across the cerebral cortex within individuals with schizophrenia

Rebecca DeGiosio1, Ryan M Kelly2, Adam M DeDionisio1

  • 1University of Pittsburgh Department of Psychiatry, Pittsburgh, PA, USA.

NPJ Schizophrenia
|August 30, 2019
PubMed

Insights

Schizophrenia (SZ) is associated with reduced microtubule-associated protein 2 (MAP2) immunoreactivity (IR) across multiple brain regions. This MAP2-IR deficit is consistent within individuals, suggesting widespread pathology in schizophrenia.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Cell Biology

Background:

  • Previous studies indicate reduced microtubule-associated protein 2 (MAP2) immunoreactivity (IR) in schizophrenia (SZ).
  • The regional consistency of MAP2-IR deficits within individuals with SZ remains largely uncharacterized.

Purpose of the Study:

  • To investigate the pattern of MAP2-IR across distinct cortical regions in individuals with and without SZ.
  • To determine if MAP2-IR deficits in SZ are regionally specific or widespread within an individual.

Main Methods:

  • Quantitative fluorescence microscopy was used to measure MAP2-IR in deep layer 3 of the dorsolateral prefrontal cortex (DLPFC), lateral intraparietal cortex (LIP), and primary visual cortex (V1).
  • Postmortem brain tissue from 20 pairs of SZ subjects and matched nonpsychiatric comparison (NPC) subjects was analyzed.

Main Results:

  • Significantly lower MAP2-IR was observed in SZ subjects compared to NPC subjects across all three regions.
  • No significant region-by-diagnosis interaction was found, indicating consistent deficits.
  • Within-pair ratios of MAP2-IR were significantly correlated across the DLPFC, LIP, and V1.

Conclusions:

  • MAP2-IR deficits in schizophrenia are not region-specific but are consistent across multiple neocortical areas within individuals.
  • These findings suggest a generalized pathology affecting MAP2 in SZ.
  • The consistent pattern of MAP2-IR deficits has implications for understanding schizophrenia pathophysiology and developing targeted therapies.

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