Related Experiment Video

Updated: Aug 15, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Myelin-associated mRNA and protein expression deficits in the anterior cingulate cortex and hippocampus in elderly

Stella Dracheva1, Kenneth L Davis, Benjamin Chin

  • 1Department of Psychiatry, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.

Neurobiology of Disease
|October 11, 2005
PubMed

Insights

Schizophrenia is linked to oligodendrocyte and myelin-related (OMR) gene deficits, particularly in the hippocampus and anterior cingulate cortex. These deficits are brain-region specific, suggesting shared regulatory elements influence affected OMR genes.

Area of Science:

  • Neuroscience
  • Molecular Psychiatry
  • Genetics

Background:

  • Previous studies suggest oligodendrocyte and myelin-related (OMR) deficits in schizophrenia.
  • The precise magnitude and brain-region specificity of these deficits remain unclear.

Purpose of the Study:

  • To quantitatively assess OMR gene expression deficits in schizophrenia.
  • To determine the brain-region specificity of these deficits.
  • To investigate interrelationships among OMR gene expression levels.

Main Methods:

  • Quantitative analysis of mRNA expression for key OMR genes (MAG, CNP, SOX10, CLDN11, PMP22, MBP, MOBP).
  • Analysis of protein expression for CNP.
  • Brain tissue samples from the hippocampus, anterior cingulate cortex, and putamen of schizophrenia patients.
  • Correlation and factor analyses to examine gene expression interrelationships.

Main Results:

  • Reduced mRNA expression of MAG, CNP, SOX10, CLDN11, and PMP22 was observed in the hippocampus and anterior cingulate cortex, but not the putamen.
  • CNP protein expression was decreased in the hippocampus but not the putamen.
  • Genes with differential expression loaded onto separate factors, distinct from those without significant changes (MBP, MOBP).

Conclusions:

  • OMR gene and protein expression deficits in schizophrenia are brain-region specific.
  • Affected OMR genes may be influenced by shared regulatory elements.

Related Concept Videos

Biological Causes of Schizophrenia01:29

Biological Causes of Schizophrenia

Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...