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Summary
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Behavioural-variant frontotemporal dementia (bvFTD) is linked to longer intrinsic neural timescales in interoception, indicating altered bodily signal processing. This dysfunction may explain complex behaviours in bvFTD patients.

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Area of Science:

  • Neuroscience
  • Cognitive Science
  • Neurology

Background:

  • Behavioural-variant frontotemporal dementia (bvFTD) is characterized by dysfunctional allostatic-interoception, an altered processing of bodily signals.
  • Previous research on interoception in bvFTD primarily used static measures, failing to capture the dynamic nature of neural processing.
  • Intrinsic neural timescales, representing temporal information processing durations, offer a dynamic measure of interoception.

Purpose of the Study:

  • To investigate intrinsic neural timescales of interoception in bvFTD patients.
  • To compare interoceptive timescales between bvFTD patients, Alzheimer's disease (AD) patients, and healthy controls.
  • To explore the relationship between altered interoceptive timescales and cognitive/social functioning in bvFTD.

Main Methods:

  • 112 participants (31 bvFTD, 35 AD, 46 controls) underwent EEG and ECG during an interoception/exteroception task.
  • Intrinsic neural timescales were quantified using the autocorrelation window (ACW) of EEG signals.
  • Spatiotemporal clustering, HEP modulation analysis, and voxel-based morphometry were employed.

Main Results:

  • bvFTD patients exhibited longer interoceptive-ACWs in fronto-temporal and parietal regions compared to controls.
  • AD patients showed longer interoceptive-ACWs in central and occipitoparietal regions.
  • In bvFTD, longer interoceptive-ACW correlated with poorer sociocognitive performance, independent of HEP modulation.

Conclusions:

  • Altered intrinsic neural timescales of interoception represent a core deficit in bvFTD, reflecting dysfunctional allostatic-interoception.
  • These dynamic interoceptive alterations may underpin the complex behavioral symptoms observed in bvFTD.
  • Findings suggest distinct neural disruption patterns in bvFTD versus AD and support synergistic models of brain disease.