Cardiorespiratory Fitness and Preserved Medial Temporal... : Alzheimer Disease & Associated Disorders (original) (raw)

Original Articles

Honea, Robyn A. DPhil*; Thomas, George P. BS*; Harsha, Amith MS*; Anderson, Heather S. MD*; Donnelly, Joseph E. PhD†; Brooks, William M. MD* ‡; Burns, Jeffrey M. MD*

*Department of Neurology

‡Hoglund Brain Imaging Center, University of Kansas School of Medicine, Kansas City

†Center for Physical Activity and Weight Management, University of Kansas, Lawrence, KS

Supported by Grants R03AG026374 and R21 AG029615 from the National Institutes of Aging and K23 NS058252 from the National Institute on Neurological Disorders and Stroke. The University of Kansas General Clinical Research Center (M01RR023940) provided essential space, expertize, and nursing support. The Hoglund Brain Imaging Center is supported by Grant C76 HF00201 and Dr Brooks is supported by NS039123 and AG026482.

Reprints: Robyn A. Honea, DPhil, Department of Neurology, University of Kansas School of Medicine, 2100 West 36th Avenue, Suite 110, Kansas City, KS 66160 (e-mail: [email protected]).

Received for publication October 9, 2008; accepted December 31, 2008

The statistical analysis was completed by Robyn Honea, DPhil.

Conflict of Interest/Disclosures: There are no financial disclosures relevant to this study. Coauthors have no disclosures or conflicts of interest.

Abstract

Exercise and cardiorespiratory (CR) fitness may moderate age-related regional brain changes in nondemented (ND) older adults. The relationship of fitness to Alzheimer disease (AD)-related brain change is understudied, particularly in the hippocampus, which is disproportionately affected in early AD. The role of apolipoprotein E4 (apoE4) genotype in modulating this relationship is also unknown. ND (n=56) and early-stage AD patients (n=61) over the age of 65 years had magnetic resonance imaging and CR fitness assessments. Voxel-based morphometry techniques were used to identify AD-related atrophy. We analyzed the relationship of CR fitness with white and gray matter within groups, assessed fitness-related brain volume change in areas most affected by AD-related atrophy, and then analyzed differential fitness-brain relationships between apoE4 carriers. Atrophy was present in the medial temporal, temporal, and parietal cortices in patients with mild AD. There was a significant positive correlation of CR fitness with parietal and medial temporal volume in AD patients. ND patients did not have a significant relationship between brain volume and CR fitness in the global or small volume correction analyses. There was not a significant interaction for fitness×apoE4 genotype in either group. In early-stage AD, CR fitness is associated with regional brain volumes in the medial-temporal and parietal cortices suggesting that maintaining CR fitness may modify AD-related brain atrophy.