Current literature suggests that the pathology of schizophrenia (SCZ) has developmental origins. However, the neurodevelopmental theory of SCZ cannot solely explain progressive neurodegenerative processes in the illness. There is evidence of accelerated cognitive decline and increased risk of dementia in elderly patients with SCZ. Investigating β-amyloid (Aβ), we conducted a systematic review focusing on Aβ in patients with SCZ. An OVID literature search using PsychINFO, Medline, and Embase databases was conducted, looking for studies that compared Aβ levels between patients with SCZ and either elderly control subjects, patients with Alzheimer disease (AD), or patients with other psychiatric illnesses. Among 14 identified studies, 11 compared Aβ between SCZ and elderly control subjects, 7 between SCZ and AD, and 3 between SCZ and other psychiatric illnesses. As a result, no evidence was found suggesting that Aβ levels differ in patients with SCZ from elderly control subjects or patients with other psychiatric illnesses. All seven studies reported lower cortical Aβ in patients with SCZ than patients with AD. Furthermore, three of the four studies, which investigated the relationship between Aβ and cognitive impairment in SCZ, observed no association between two factors. The limitations of the included studies are small sample sizes, the inclusion of cerebrospinal fluid Aβ or postmortem plaques rather than cortical Aβ assessment in vivo, and the investigation of different brain regions. In conclusion, Aβ deposition is not associated with cognitive decline in late-life SCZ. Future studies should investigate other neurodegenerative indicators in SCZ to better understand the pathophysiologic mechanisms underlying this illness.
Keywords: Alzheimer disease; cognitive decline; neurodegeneration; schizophrenia; β-Amyloid.
Copyright © 2016 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.