No abstract

Smoking during adolescence may promote nicotine dependence later on in life. Therefore, it is extremely important to study the neural mechanisms of adolescent smokers. As inhibition control is emphasized in several contemporary theoretical models of addiction, in the current study, we focused on the electrophysiological evidence of inhibition control deficits in adolescent smokers. By using relatively homogenous groups of adolescent smokers (n = 18) and matched nonsmokers (n = 18), we employed event-related potentials (ERP) to investigate the N200 and P300 amplitude and latency differences during a Go/NoGo task between the adolescent smokers and nonsmokers. Relative to nonsmokers, more NoGo response errors, reduced NoGo P300 amplitude, and longer P300 latency were observed in adolescent smokers. Correlation analysis revealed that the NoGo P300 amplitudes were significantly correlated with NoGo errors in both adolescent smokers and nonsmokers. Our findings provided direct electrophysiological evidence for inhibitory control impairments in adolescent smokers. It is hoped that our results may enhance understanding of the pathology of inhibitory control in adolescent smokers.

New findings relating to the clinical, genetic and molecular bases of neurodegenerative disorders have led to a shift away from traditional nomenclatures of clinical syndromes. Historically, frontotemporal lobar degeneration (FTLD), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) were classified on the basis of distinct clinical and pathological features. In recent years, however, advances in molecular and genetic research have led clinicians to suggest that the similar etiologies of the three disorders warrant their amalgamation into a single disorder with three subtypes. In this Review, we consider the utility and validity of combining FTLD, CBD and PSP. The earliest reports of these disorders demonstrate their distinctiveness, whereas recent findings challenge traditional nomenclatures by showing etiological overlap. For example, tau inclusions have been confirmed in patients with CBD and those with PSP, and in some patients with FTLD, implying that all three disorders are 'tauopathies'. Furthermore, most patients with progressive nonfluent aphasia, a subtype of FTLD, show PSP or CBD post-mortem. Even tau-related cases of FTLD, CBD and PSP are distinguishable on the basis of other criteria, however, and many FTLD cases do not show tau pathology. We argue, therefore, that FTLD, CBD and PSP should be considered as pathologically similar but distinct syndromes. New research criteria for CBD and PSP should note that progressive nonfluent aphasia is often a precursor of these conditions.