Journal
HIPPOCAMPUS
Volume 31, Issue 3, Pages 305-320Publisher
WILEY
DOI: 10.1002/hipo.23290
Keywords
cardiorespiratory fitness; cognitive reserve; hippocampus; memory; mild cognitive impairment; neuroimaging
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Funding
- National Institute for Psychobiology in Israel, Hebrew University of Jerusalem
- Israel Science Foundation
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This study suggests that maximal aerobic capacity (MAC) may be associated with hippocampal-related cognitive reserve in aMCI patients by altering the relationship between hippocampal-related structural deterioration and cognitive function. Additionally, MAC is found to be associated with increased capacity to recruit neural resources during increased cognitive demands.
Maximal aerobic capacity (MAC) has been associated with preserved neural tissue or brain maintenance (BM) in healthy older adults, including the hippocampus. Amnestic mild cognitive impairment (aMCI) is considered a prodromal stage of Alzheimer's disease. While aMCI is characterized by hippocampal deterioration, the MAC-hippocampal relationship in these patients is not well understood. In contrast to healthy individuals, neurocognitive protective effects in neurodegenerative populations have been associated with mechanisms of cognitive reserve (CR) altering the neuropathology-cognition relationship. We investigated the MAC-hippocampal relationship in aMCI (n = 29) from the perspectives of BM and CR mechanistic models with structural MRI and a memory fMRI paradigm using both group-level (higher-fit patients vs. lower-fit patients) and individual level (continuous correlation) approaches. While MAC was associated with smaller hippocampal volume, contradicting the BM model, higher-fit patients demonstrated statistically significant lower correlation between hippocampal volume and memory performance compared with the lower-fit patients, supporting the model of CR. In addition, while there was no difference in brain activity between the groups during low cognitive demand (encoding of familiar stimuli), higher MAC level was associated with increased cortical and sub-cortical activation during increased cognitive demand (encoding of novel stimuli) and also with bilateral hippocampal activity even when controlling for hippocampal volume, suggesting for an independent effect of MAC. Our results suggest that MAC may be associated with hippocampal-related cognitive reserve in aMCI through altering the relationship between hippocampal-related structural deterioration and cognitive function. In addition, MAC was found to be associated with increased capacity to recruit neural resources during increased cognitive demands.
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