A Study of Localized Spontaneous Activity Changes in Cerebral White Matter in Adolescent Smoking Addiction.

Introduction: Previous research has primarily concentrated on alterations in spontaneous brain activity within the gray matter of young smokers; however, the influence of nicotine addiction on spontaneous brain activity in the white matter was unknown.

Methods: The current study encompassed 45 male smokers and 45 male non-smokers. Regional Homogeneity (ReHo) and Amplitude of Low-Frequency Fluctuations (ALFF) analyses were applied to examine regional neural activity in the white matter. Voxel-wise two-sample t-tests were employed to detect differences between the two groups, significance was determined using an FDR correction (voxel-level threshold: p<.001; cluster-level q < 0.05). Pearson correlation was conducted to assess the relationships between ReHo/ALFF and the Fagerström Test for Nicotine Dependence (FTND).

Results: Smokers exhibited significantly decreased ReHo in the corticospinal tract (CST) and the splenium of the corpus callosum (SCC),while increased ReHo was observed in the bilateral posterior thalamic radiation (PTR). Decreased ALFF was observed in the right superior corona radiata, the SCC, and the left medial lemniscus. Correlation analysis showed that the ReHo value in the CST was negatively correlated with FTND (r = -0.353, p=.017).

Conclusions: This study found that there were abnormalities in the local functional activity of white matter in young smokers; and the aberrant activity was related the severity of smoking. The findings may provide additional evidence for understanding nicotine addiction.

Implications: This study reveals abnormal patterns of localized spontaneous neural activity in the white matter of young smokers. Given the developmental trajectory of the brain, alterations in white matter functional activity may precede those in gray matter. These findings suggest that localized white matter functional changes could serve as early biomarkers of young nicotine addicts and expand our understanding of its underlying neurobiological mechanisms.