Literature DB >> 27717834

Does medial temporal lobe thickness mediate the association between risk factor burden and memory performance in middle-aged or older adults with metabolic syndrome?

Elissa C McIntosh1, Aaron Jacobson1, Nobuko Kemmotsu2, Ekarin Pongpipat1, Erin Green3, Lori Haase4, Claire Murphy5.   

Abstract

Metabolic syndrome (MetS) is a cluster of cardiovascular and metabolic abnormalities that together may increase the risk of developing cognitive decline and dementia; however, the neural substrate is incompletely understood. We investigated cortical thickness in the medial temporal lobe (MTL), hippocampal volume, as well as relationships among metabolic risk factor burden, structure and memory performance. Path-analytic models were tested to explore the relations between MetS risk factor, structure and memory performance. Participants were 65 non-demented, middle-aged and older adults, 34 with and 31 without metabolic syndrome. We analyzed archival T1-weighted magnetic resonance imaging (MRI) acquired at 3T and Total Recall and Delayed Recall scores from the Brief Visuospatial Memory Test Revised (BVMT-R). Middle-aged adults with MetS showed less MTL thickness, particularly in entorhinal cortex; while older adults showed a trend for left hippocampal volume loss. Lower MTL thickness, particularly in entorhinal cortex, was associated with greater metabolic risk factor burden in middle-aged adults. In older adults, hippocampal volume was associated with Total Recall and Delayed Recall, while in middle-age entorhinal cortical thickness mediated the association between metabolic disease burden and episodic memory function. The differential findings in middle-aged and older adults with MetS contribute to an understanding of the relationships between metabolic syndrome, structural changes in the brain and increased risk for cognitive decline. Copyright Â
© 2016 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.

Entities:  

Keywords:  Entorhinal cortical thickness; MRI; Medial temporal lobe; Memory; Metabolic syndrome

Mesh:

Year:  2016        PMID: 27717834      PMCID: PMC6021126          DOI: 10.1016/j.neulet.2016.10.010

Source DB:  PubMed          Journal:  Neurosci Lett        ISSN: 0304-3940            Impact factor:   3.046


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