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Gene expression signature is shared by patients with Alzheimer’s disease and schizophrenia at the superior temporal gyrus
Author(s) -
Horesh Y.,
Katsel P.,
Haroutunian V.,
Domany E.
Publication year - 2011
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2010.03166.x
Subject(s) - neuropathology , schizophrenia (object oriented programming) , neuroscience , middle temporal gyrus , temporal cortex , disease , medicine , hippocampus , alzheimer's disease , superior frontal gyrus , superior temporal gyrus , dentate gyrus , gyrus , psychiatry , psychology , pathology , functional magnetic resonance imaging
Background: Alzheimer’s disease and Schizophrenia are two common diseases of the brain with significant differences in neuropathology, etiology and symptoms. This dissimilarity in the two diseases makes a comparison of the two ideal for detecting molecular substrates that are common to brain disorders in general. Methods: In this study, we compared gene expression profiles across multiple brain areas, taken postmortem from patients with well‐characterized Alzheimer’s disease and Schizophrenia, and from cognitively normal control group with no neuro‐ or psychopathology. Results: Although the totality of gene expression changes in the two diseases is dissimilar, a subset of genes appears to play a role in both diseases in specific brain regions. We find at Brodmann area 22, the superior temporal gyrus, a statistically significant number of genes with apparently disregulated expression in both diseases. Furthermore, we found genes that differentiate the two diseases from the control across multiple brain regions, and note that these genes were usually down‐regulated. Brodmann area 8, part of the superior frontal cortex, is relatively abundant with them. Conclusion: We show overwhelming statistical evidence for Alzheimer’s and Schizophrenia sharing a specific molecular background at the superior temporal gyrus. We suggest that impairment of the regulation of autophagy pathway is shared, in BA 22, by the two diseases.