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OBJECTIVE: Internet delivery of behavioural weight control interventions offers potential for broad geographic reach and accessibility, but weight losses online fall short of those produced with the same programme delivered in-person. This pilot study examined feasibility and preliminary efficacy of a video-based platform for delivering weekly chat as part of a 6-month, 24-session online group behavioural weight control programme compared with the established text-based format, which has produced the best online weight losses to date. METHOD: Women with obesity (N = 32) were randomized to either (a) weekly video group chat sessions and provided with a cellular-enabled scale (Video) or (b) Text-based weekly chat sessions and given a digital scale (Text) and followed for 6 months to determine weight loss and treatment engagement. RESULTS: Women randomized to the ideo condition lost more weight than those in the Text condition (-5.0 ± 6.0% vs. -3.0 ± 4.1%, respectively) at 6 months, although the difference was not statistically significant. However, women in the Video condition had significantly greater treatment engagement, with greater self-monitoring and website utilization than those in the Text condition. CONCLUSIONS: Videoconference delivery of group-based online weight control accompanied by a cellular-connected scale may promote greater treatment engagement and weight loss than text-based chat. A larger, adequately powered study is warranted to determine which elements drive these enhanced treatment outcomes.
RESUMO
Individuals with familial Parkinson's disease (PD) due to a monogenic defect can show considerable clinical and neuropathological variability. To identify factors underlying this variability, histopathological analysis was performed in two clinically different A53T alpha-synuclein heterozygotes from Family H, a multigenerational alpha-synuclein A53T kindred. To determine whether additional genetic factors could contribute to phenotypic variability, Family H and another multigenerational A53T kindred were analyzed for parkin polymorphisms. We identified a previously described variant in parkin exon 4 associated with increased PD risk (S167N). The two A53T heterozygotes had markedly different neuropathology and different parkin genotypes: A N167 homozygote had early onset rapidly progressive disease, early dementia, myoclonus and sleep disorder, while a S167 homozygote had late onset, slowly progressive disease and late dementia. Both had brainstem, cortical, and intraneuritic Lewy bodies (LB). The N167 individual had widespread cortical neurofibrillary degeneration, while the S167 individual had only medial temporal lobe neurofibrillary degeneration. The N167 individual had severe neuronal loss in CA2 associated with Lewy neurites (LN), while the S167 individual had severe neuronal loss in CA1 associated with TDP-43 immunoreactive neuronal inclusions. These findings implicate TDP-43 in the pathology of familial PD and suggest that parkin may act as a modifier of the A53T alpha-synuclein phenotype of familial PD. Furthermore, they suggest a mechanism by which a rare genetic variant that is associated with a minor increase of PD risk in the heterozygous state may, in the homozygous state, exacerbate a disease phenotype associated with a highly penetrant dominant allele.