Performance on the cogstate brief battery is related to amyloid levels and hippocampal volume in very mild dementia

Author Identifier

Simon Laws

Document Type

Journal Article

Publication Title

Journal of Molecular Neuroscience




School of Medical and Health Sciences / Centre of Excellence for Alzheimer's Disease Research and Care / Centre for Precision Health




Edith Cowan University

National Health and Medical Research Council

Australian Research Council

Further funding information :

Grant Number

NHMRC - ARC Number : APP1111603


Lim, Y. Y., Villemagne, V. L., Laws, S. M., Pietrzak, R. H., Ames, D., Fowler, C., . . . Maruff, P. (2016). Performance on the cogstate brief battery is related to amyloid levels and hippocampal volume in very mild dementia. Journal of Molecular Neuroscience, 60(3), 362-370.


In a group of older adults with very mild dementia, we aimed to characterize the nature and magnitude of cognitive decline as measured by the Cogstate Brief Battery, in relation to Aβ levels and hippocampal volume. Participants were characterized according to their status on the Clinical Dementia Rating (CDR) scale. A total of 308 individuals who were CDR 0 and had low cerebral Aβ levels (Aβ−), 32 individuals who were Aβ− and CDR 0.5, and 43 individuals who were Aβ+ and CDR 0.5 were included in this study. Participants completed the CogState brief battery at baseline, and at 18-, 36-, 54- and 72-month follow-up. Linear mixed model analyses indicated that relative to the Aβ− CDR 0 group, the Aβ+ CDR 0.5 group showed increased rates of memory decline and hippocampal volume loss. However, compared to the Aβ− CDR 0 group, the Aβ− CDR 0.5 group showed no changes in cognitive function or hippocampal volume over 72 months. The results of this study confirm that in individuals with very mild dementia, who also have biomarker confirmation of Aβ+, changes in cognitive function manifest primarily as deterioration in memory processing, and this is associated with hippocampal volume loss. Conversely, the absence of any cognitive decline or loss in hippocampal volume in individuals with very mild dementia but who are Aβ− suggests that some other non-AD disease process may underlie any static impairment in cognitive function.



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