Format

Send to

Choose Destination
Psychiatry Res. 2016 Jan 30;235:200-2. doi: 10.1016/j.psychres.2015.12.007. Epub 2015 Dec 8.

C9orf72 repeat expansions that cause frontotemporal dementia are detectable among patients with psychosis.

Author information

1
Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, United States.
2
Departments of Psychiatry and Neurology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States.
3
Memory and Aging Center/Sandler Neurosciences Center, University of California San Francisco, San Francisco, CA, United States.
4
Departments of Psychiatry and Neurology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States. Electronic address: gcoppola@ucla.edu.
5
Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, United States; Department of Human Genetics, University of Pittsburgh, Graduate School of Public Health, Pittsburgh, PA, United States. Electronic address: nimga@pitt.edu.

Abstract

A pathologic hexanucleotide repeat expansion in C9orf72 causes frontotemporal dementia (FTD) or amyotrophic lateral sclerosis (ALS). Behavioral abnormalities can also occur among mutation carriers with FTD, but it is uncertain whether such mutations occur among persons with psychoses per se. Among participants in a genetic study of psychoses (N=739), two pairs of related individuals had C9orf72 expansions, of whom three were diagnosed with schizophrenia (SZ) / schizoaffective disorder (SZA), but their clinical features did not suggest dementia or ALS. A few patients with SZ/SZA carry C9orf72 repeat expansions; such individuals are highly likely to develop FTD/ALS.

KEYWORDS:

Dementia; Schizoaffective disorder; Schizophrenia

PMID:
26723138
PMCID:
PMC4724461
DOI:
10.1016/j.psychres.2015.12.007
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center