Abstract
Introduction: Functional imaging studies have demonstrated the recruitment of additional neural resources as a possible mechanism to compensate for age and Alzheimer’s disease (AD)-related cerebral pathology, the efficacy of which is potentially modulated by underlying structural network connectivity. Additionally, structural network efficiency (SNE) is associated with intelligence across the lifespan, which is a known factor for resilience to cognitive decline. We hypothesized that SNE may be a surrogate of the physiological basis of resilience to cognitive decline in elderly persons without dementia and with age- and AD-related cerebral pathology.Methods: We included 85 cognitively normal elderly subjects or mild cognitive impairment (MCI) patients submitted to baseline diffusion imaging, liquor specimens, amyloid-PET and longitudinal cognitive assessments. SNE was calculated from baseline MRI scans using fiber tractography and graph theory. Mixed linear effects models were estimated to investigate the association of higher resilience to cognitive decline with higher SNE and the modulation of this association by increased cerebral amyloid, liquor tau or WMHV. Results: For the majority of cognitive outcome measures, higher SNE was associated with higher resilience to cognitive decline (p-values: 0.011–0.039). Additionally, subjects with higher SNE showed more resilience to cognitive decline at higher cerebral amyloid burden (p-values: <0.001–0.036) and lower tau levels (p-values: 0.002–0.015).Conclusion: These results suggest that SNE to some extent may quantify the physiological basis of resilience to cognitive decline most effective at the earliest stages of AD, namely at increased amyloid burden and before increased tauopathy.
Highlights
Functional imaging studies have demonstrated the recruitment of additional neural resources as a possible mechanism to compensate for age and Alzheimer’s disease (AD)-related cerebral pathology, the efficacy of which is potentially modulated by underlying structural network connectivity
All mixed-effects regression models that best explained the data for each cognitive measure according to conditional AIC (cAIC) contained the term for general resilience (T*structural network efficiency (SNE)) as well as a term for dynamic resilience at elevated amyloid (T*SNE*AV45) and limited resilience at elevated tau levels (T*SNE*TAU)
The main results of this study indicate that in a population of non-demented elderly with varying amounts of age- and AD-related cerebral pathology, higher efficiency of the cerebral network may be associated with more resilience to cognitive decline
Summary
Functional imaging studies have demonstrated the recruitment of additional neural resources as a possible mechanism to compensate for age and Alzheimer’s disease (AD)-related cerebral pathology, the efficacy of which is potentially modulated by underlying structural network connectivity. We hypothesized that SNE may be a surrogate of the physiological basis of resilience to cognitive decline in elderly persons without dementia and with age- and AD-related cerebral pathology. Structural Network Predicts Cognitive Decline or compensate cerebral pathology, commonly termed reserve or—more generally—resilience (Yaffe et al, 2011; Barulli and Stern, 2013; Cabeza et al, 2018; Wolf et al, 2018). The identification and quantification of an MRI-based surrogate of the physiological basis of this resilience could complement and significantly improve individual predictions of cognitive decline based on cerebral pathology. In higher age and in the presence of cerebral pathology, the brain seems to recruit more neural resources for given cognitive tasks as compared to younger subjects or those with less pathology present, which may be a resilience mechanism (Sebastian et al, 2013; Reuter-Lorenz and Park, 2014; Stargardt et al, 2015; Fernández-Cabello et al, 2016)
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