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Cognitive reserve attenuates age-related cognitive decline in the context of putatively accelerated brain ageing in schizophrenia-spectrum disorders

Published online by Cambridge University Press:  09 July 2019

Tamsyn E. Van Rheenen*
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia Centre for Mental Health, Faculty of Health, Arts and Design, School of Health Sciences, Swinburne University, Melbourne, Australia
Vanessa Cropley
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia Centre for Mental Health, Faculty of Health, Arts and Design, School of Health Sciences, Swinburne University, Melbourne, Australia
Birgitte Fagerlund
Affiliation:
Center for Neuropsychiatric Schizophrenia Research and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Center, Glostrup, Denmark Department of Psychology, University of Copenhagen, Copenhagen, Denmark
Cassandra Wannan
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia
Jason Bruggemann
Affiliation:
School of Psychiatry, University of New South Wales, New South Wales, Australia Neuroscience Research Australia, New South Wales, Australia
Rhoshel K. Lenroot
Affiliation:
School of Psychiatry, University of New South Wales, New South Wales, Australia Neuroscience Research Australia, New South Wales, Australia
Suresh Sundram
Affiliation:
Florey Institute of Neuroscience and Mental Health, Melbourne, Australia Department of Psychiatry, School of Clinical Sciences, Monash University, Clayton, Australia Mental Health Program, Monash Health, Clayton, Victoria, Australia
Cynthia Shannon Weickert
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia School of Psychiatry, University of New South Wales, New South Wales, Australia Neuroscience Research Australia, New South Wales, Australia Department of Neuroscience & Physiology, Upstate Medical University, Syracuse, New York13210, USA
Thomas W. Weickert
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia School of Psychiatry, University of New South Wales, New South Wales, Australia Neuroscience Research Australia, New South Wales, Australia
Andrew Zalesky
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia Department of Electrical and Electronic Engineering, University of Melbourne, VIC, Australia
Chad A. Bousman
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia Florey Institute of Neuroscience and Mental Health, Melbourne, Australia Departments of Medical Genetics, Psychiatry, and Physiology & Pharmacology, University of Calgary, Calgary, AB, Canada
Christos Pantelis
Affiliation:
Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australia Florey Institute of Neuroscience and Mental Health, Melbourne, Australia Department of Electrical and Electronic Engineering, University of Melbourne, VIC, Australia
*
Author for correspondence: Tamsyn E. Van Rheenen, E-mail: [email protected]

Abstract

Background

In schizophrenia, relative stability in the magnitude of cognitive deficits across age and illness duration is inconsistent with the evidence of accelerated deterioration in brain regions known to support these functions. These discrepant brain–cognition outcomes may be explained by variability in cognitive reserve (CR), which in neurological disorders has been shown to buffer against brain pathology and minimize its impact on cognitive or clinical indicators of illness.

Methods

Age-related change in fluid reasoning, working memory and frontal brain volume, area and thickness were mapped using regression analysis in 214 individuals with schizophrenia or schizoaffective disorder and 168 healthy controls. In patients, these changes were modelled as a function of CR.

Results

Patients showed exaggerated age-related decline in brain structure, but not fluid reasoning compared to controls. In the patient group, no moderation of age-related brain structural change by CR was evident. However, age-related cognitive change was moderated by CR, such that only patients with low CR showed evidence of exaggerated fluid reasoning decline that paralleled the exaggerated age-related deterioration of underpinning brain structures seen in all patients.

Conclusions

In schizophrenia-spectrum illness, CR may negate ageing effects on fluid reasoning by buffering against pathologically exaggerated structural brain deterioration through some form of compensation. CR may represent an important modifier that could explain inconsistencies in brain structure – cognition outcomes in the extant literature.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2019

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