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A major challenge in the cognitive training field is inducing broad, far‐transfer training effects. Thus far, little is known about the neural mechanisms underlying broad training effects. Here, we tested a set of competitive hypotheses regarding the role of brain integration versus segregation underlying the broad training effect. We retrospectively analyzed data from a randomized controlled trial comparing neurocognitive effects of vision‐based speed of processing training (VSOP) and an active control consisting of mental leisure activities (MLA) in older adults with MCI. We classified a subset of participants in the VSOP as learners, who showed improvement in executive function and episodic memory. The other participants in the VSOP (i.e., VSOP non‐learners) and a subset of participants in the MLA (i.e., MLA non‐learners) served as controls. Structural brain networks were constructed from diffusion tensor imaging. Clustering coefficients (CCs) and characteristic path lengths were computed as measures of segregation and integration, respectively. Learners showed significantly greater global CCs after intervention than controls. Nodal CCs were selectively enhanced in cingulate cortex, parietal regions, striatum, and thalamus. Among VSOP learners, those with more severe baseline neurodegeneration had greater improvement in segregation after training. Our findings suggest broad training effects are related to enhanced segregation in selective brain networks, providing insight into cognitive training related neuroplasticity.

Effective learning in old age, particularly in those at risk for dementia, is essential for prolonging independent living. Individual variability in learning, however, is remarkable; that is, months of cognitive training to improve learning may be beneficial for some individuals but not others. So far, little is known about which neurophysiological mechanisms account for the observed variability in learning induced by cognitive training in older adults. By combining Lövdén et al.'s (2010, A theoretical framework for the study of adult cognitive plasticity. Psychological Bulletin , 136 , 659–676) framework proposing the role of adaptation capacity in neuroplasticity and a neurovisceral integration model of the relationship between autonomic nervous system (ANS) and brain with a novel shapelet analytical approach that allows for accurate and interpretable analysis of time series data, we discovered an acute, ECG‐derived ANS segment in response to cognitive training tasks at baseline that predicted learning outcomes from a 6‐week cognitive training intervention. The relationship between the ANS segment and learning was robust in both cross‐participant and cross‐task analyses among a group of older adults with amnestic mild cognitive impairment. Furthermore, the revealed ANS shapelet significantly predicted training‐induced neuroplasticity in the dorsal anterior cingulate cortex and select frontal regions during task fMRI. Across outcome measures, individuals were less likely to prospectively benefit from the cognitive training if their ECG data were more similar to this particular ANS segment at baseline. Our findings are among the first empirical evidence to confirm that adaptation capacity, indexed by ANS flexibility, predicts individual differences in learning and associated neuroplasticity beyond individual characteristics (e.g., age, education, neurodegeneration, total training).

Highlights Supernormals maintain a unique structural connectome that remains stable over time. The “Supernormals structural connectome” predicts AD progression. Cingulate to precuneus connection contributes the most to predicting AD pathology.

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The relationship between Alzheimer’s disease (AD) pathology and cognitive decline is an important topic in the aging research field. Recent studies suggest that memory deficits are more susceptible to phosphorylated tau (Ptau) than amyloid-beta. However, little is known regarding the neurocognitive mechanisms linking Ptau and memory-related decline. Here, we extracted data from Alzheimer’s Disease Neuroimaging Initiative (ADNI) participants with cerebrospinal fluid (CSF) Ptau collected at baseline, diffusion tensor imaging measure twice, 2 year apart, and longitudinal memory data over 5 years. We defined three age- and education-matched groups: Ptau negative cognitively unimpaired, Ptau positive cognitively unimpaired, and Ptau positive individuals with mild cognitive impairment. We found the presence of CSF Ptau at baseline was related to a loss of structural stability in medial temporal lobe connectivity in a way that matched proposed disease progression, and this loss of stability in connections known to be important for memory moderated the relationship between Ptau accumulation and memory decline.

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