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      Hippocampal atrophy and intrinsic brain network alterations relate to impaired capacity for mind wandering in neurodegeneration

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      bioRxiv

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          Abstract

          Mind wandering represents the human capacity for internally focussed thought, and relies upon dynamic interactions between default and frontoparietal networks. The majority of studies in the field have characterised mind wandering in healthy people, yet there is limited understanding of how this capacity is affected in clinical populations. The present study used a validated thought sampling task, to probe the capacity for mind wandering in two neurodegenerative disorders; the behavioural variant of frontotemporal dementia (n=28) and Alzheimer's disease (n=22), compared to healthy older controls (n=28). These disorders were selected due to their canonical profiles of neural dysfunction across key sites of the default and frontoparietal networks. Behaviourally, mind wandering frequency was found to be reduced in the patient groups, leading to an increase in stimulus-bound thoughts. These behavioural profiles were associated with distinct regions of grey matter loss, as revealed by voxel-based morphometry, predominantly in the hippocampal complex and striatum. Resting state functional connectivity further revealed associations between impaired mind wandering performance and altered connectivity within and between regions of the frontoparietal and default networks. Together, these findings are the first to describe altered mind wandering in neurodegenerative disorders, which was associated with hippocampal atrophy and aberrations in the functional integrity of the default and frontoparietal networks. These results corroborate current theoretical frameworks emphasising that cooperation between default and frontoparietal regions is critical for producing and sustaining internally focussed thought. Notably this study reveals a new dimension of cognitive dysfunction not previously documented in neurodegenerative disorders.

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          Author and article information

          Journal
          bioRxiv
          September 26 2017
          Article
          10.1101/194092
          51bed754-ad18-4e34-90a8-972e3913c6c7
          © 2017
          History

          Molecular medicine,Neurosciences
          Molecular medicine, Neurosciences

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