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Area of Science:

  • Neuroscience
  • Neurodevelopmental Disorders
  • Cognitive Neuroscience

Background:

  • Neurofibromatosis type 1 (NF1) is a genetic disorder associated with cognitive deficits, particularly in working memory.
  • Atypical brain activation patterns are observed in individuals with NF1 during working memory tasks.
  • Frontoparietal effective connectivity alterations are hypothesized to underlie these working memory difficulties.

Purpose of the Study:

  • To investigate alterations in frontoparietal effective connectivity during working memory in adolescents with NF1.
  • To specifically examine self-connections (intrinsic inhibitory influences) within the frontoparietal network.
  • To test the hypothesis that NF1 is characterized by greater inhibitory intrinsic self-connections.

Main Methods:

  • Functional magnetic resonance imaging (fMRI) was used in 43 adolescents with NF1 and 26 controls during a verbal working memory task.
  • Dynamic causal modeling (DCM) was applied to estimate effective connectivity within the bilateral frontoparietal network (dlPFC, vlPFC, SPG, IPG).
  • Parametric empirical Bayes with Bayesian model reduction and leave-one-out cross-validation were employed to analyze group differences and generalizability.

Main Results:

  • NF1 participants showed greater endogenous self-connectivity in the left dorsolateral prefrontal cortex (dlPFC) and left inferior parietal gyrus (IPG).
  • Working memory modulation revealed increased intrinsic connectivity of the left ventrolateral prefrontal cortex (vlPFC) but decreased connectivity in the left dlPFC, left superior parietal gyrus (SPG), and right IPG in the NF1 group.
  • Connectivity parameters positively correlated with diagnosis status, indicating predictive value.

Conclusions:

  • Increased endogenous self-connectivity in specific regions of NF1 participants suggests reduced regional sensitivity to inputs.
  • Working memory processing in NF1 involves complex modulatory connectivity patterns beyond simple increased inhibition.
  • Atypical adaptation to working memory demands in NF1 may stem from a discrepancy between endogenous and task-evoked connectivity patterns.