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The relationship of excess cognitive impairment in MCI and early Alzheimer's disease to the subsequent emergence of psychosis

Published online by Cambridge University Press:  25 September 2008

Elise A. Weamer
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A. Department of Neurology, University of Pittsburgh, Pittsburgh, U.S.A.
James E. Emanuel
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A.
Daniel Varon
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A.
Sachiko Miyahara
Affiliation:
Department of Epidemiology, University of Pittsburgh, Pittsburgh, U.S.A.
Patricia A. Wilkosz
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A.
Oscar L. Lopez
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A. Department of Neurology, University of Pittsburgh, Pittsburgh, U.S.A.
Steven T. DeKosky
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A.
Robert A. Sweet*
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, U.S.A. Department of Neurology, University of Pittsburgh, Pittsburgh, U.S.A. VISN 4 Mental Illness Research, Education and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA.U.S.A.
*
Correspondence should be addressed to: Robert A. Sweet, M.D., Associate Professor of Psychiatry and Neurology, Biomedical Science Tower, Rm W-1645, 3811 O'Hara Street, Pittsburgh, PA 15213–2593, U.S.A. Phone + 1 412 383 8548; Fax + 1 412 624 9910. Email: [email protected].
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Abstract

Background: Psychotic symptoms in Alzheimer disease (AD + P) identify a heritable phenotype associated with greater cognitive impairment. Knowing when the cognitive course of AD + P subjects diverges from that of subjects without psychosis would enhance understanding of how genetic variation results in AD + P and its associated cognitive burden. This study seeks to determine whether the degree of cognitive impairment and cognitive decline in early AD predicts subsequent AD + P onset.

Methods: 361 subjects with possible or probable AD or mild cognitive impairment (MCI) without psychosis were evaluated every 6 months until psychosis onset.

Results: Severity of cognitive dysfunction was a strong predictor of AD + P up to two years prior to psychosis onset. Cognition did not decline more rapidly prior to onset of AD + P.

Conclusions: Individuals who will develop AD + P already demonstrate excess cognitive impairment during the mild stages of disease. Genetic variation and brain pathophysiology may lead to a cognitive risk phenotype which is present prior to dementia onset.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2008

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