Cerebral Cortex Advance Access originally published online on September 14, 2005
Cerebral Cortex 2006 16(7):907-915; doi:10.1093/cercor/bhj036
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Feature Article |
StructureFunction Correlates of Cognitive Decline in Aging
1 Department of Psychology, Umeå University, S-901 87 Umeå, Sweden, 2 MR Research Center, Karolinska Hospital, S-171 76 Stockholm, Sweden, 3 Department of Radiation Sciences Radiation Physics, Umeå University, S-901 87 Umeå, Sweden, 4 Department of Psychology, Stockholm University, S-106 91 Stockholm, Sweden and 5 Departments of Psychology, Radiology, and Anatomy & Neurobiology, Howard Hughes Medical Institute at Washington University, St Louis, MO 63130, USA
Address correspondence to Jonas Persson, Department of Psychology, Umeå University, S-901 87 Umeå, Sweden. Email: perssonj{at}umich.edu.
To explore neural correlates of cognitive decline in aging, we used longitudinal behavioral data to identify two groups of older adults (n = 40) that differed with regard to whether their performance on tests of episodic memory remained stable or declined over a decade. Analysis of structural and diffusion tensor imaging (DTI) revealed a heterogeneous set of differences associated with cognitive decline. Manual tracing of hippocampal volume showed significant reduction in those older adults with a declining memory performance as did DTI-measured fractional anisotropy in the anterior corpus callosum. Functional magnetic resonance imaging during incidental episodic encoding revealed increased activation in left prefrontal cortex for both groups and additional right prefrontal activation for the elderly subjects with the greatest decline in memory performance. Moreover, mean DTI measures in the anterior corpus callosum correlated negatively with activation in right prefrontal cortex. These results demonstrate that cognitive decline is associated with differences in the structure as well as function of the aging brain, and suggest that increased activation is either caused by structural disruption or is a compensatory response to such disruption.
Key Words: aging compensation corpus callosum prefrontal diffusion-tensor imaging fMRI hippocampus longitudinal memory
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