Affiliations: [a] Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA | [b] Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA | [c] VISN 4 Mental Illness Research, Education and Clinical Center (MIRECC), VA Pittsburgh Healthcare System, Pittsburgh, PA, USA
Correspondence:
[*]
Correspondence to: Robert A. Sweet, M.D., Biomedical Science Tower, Rm W-1645, 3811 O'Hara Street, Pittsburgh, PA 15213-2593, USA. Tel.: +1 412 383 8548; Fax: +1 412 624 9910; E-mail: sweetra@upmc.edu.
Abstract: In and of itself, late-onset Alzheimer's disease (AD) can be a devastating illness. However, a sub-group of AD patients develop psychosis as the disease progresses. These patients have an added burden of greater cognitive impairment, higher rates of institutionalization, and higher mortality than AD patients without psychosis. While the etiopathogenesis such as psychosis in AD (AD+P) is not known, mounting evidence accrued over the past ten years indicates that AD+P represents a distinct phenotype with a genetic basis. Elucidating the genetic mechanism of AD+P is crucial if better pharmaceutical treatments are to be developed for these patients. The goal of this review is to summarize what is currently known regarding the genetic basis of psychosis in AD. Specific attention is given to familial aggregation and heritability, linkage to chromosomal loci, and associations of candidate genes of APOE and the monoamine neurotransmitter system. An erratum for this article can be found in Journal of Alzheimer's Disease 20(4), 2010, p. 1263. https://dx.doi.org/10.3233/JAD-2010-1426
