Neuronal expression of STM2 mRNA in human brain is reduced in Alzheimer's disease

Pamela J. McMillan, James B. Leverenz, Parvoneh Poorkaj, Gerard D. Schellenberg, Daniel M. Dorsa

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Mutations in the STM2 gene cause familial Alzheimer's disease (AD) in Volga Germans. To understand the function of this protein and how mutations lead to AD, it is important to determine which cell types in the brain express this gene. In situ hybridization histochemistry indicates that STM2 expression in the human brain is widespread and is primarily neuronal. In addition, STM2 mRNA is expressed in a cell line with neuronal origins. Quantification of the level of expression of the STM2 message in the basal fore brain, frontal cortex, and hippocampus reveals a significant decrease in AD-affected subjects compared to normal age-matched controls. These data suggest that downregulation of neuronal STM2 gene expression may be involved in the progression of AD.

Original languageEnglish (US)
Pages (from-to)1215-1222
Number of pages8
JournalJournal of Histochemistry and Cytochemistry
Volume44
Issue number11
DOIs
StatePublished - Nov 1996

Keywords

  • Alzheimer's disease
  • Basal forebrain
  • Frontal cortex
  • Hippocampus
  • In situ hybridization histochemistry
  • STM2

ASJC Scopus subject areas

  • Anatomy
  • Histology

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