Psychosocial interventions for caregivers of people with dementia: a systematic review.

The content of interventions for caregivers of dementia patients is highly varied. None of the reviews conducted to date have focused on evaluating the effects of the content of interventions exclusively for dementia caregivers, and this issue is not well understood. The purpose of this review was to first identify the type of components (e.g. education, counselling) that have been utilized in psychosocial/psycho-educational interventions for dementia caregivers, and to evaluate the success of the different components or combination of components in producing positive outcomes for dementia caregivers. Forty studies were included in the review. Approximately two-thirds of the interventions did not show improvements in any outcome measures. Among those studies, which did demonstrate improvements, the inclusion of social components (e.g. social support) or a combination of social and cognitive (e.g. problem solving) components seemed to be relatively effective. It is important to note, however, that these analyses were based on small numbers and the review was limited by a number of methodological issues (e.g. poor description of interventions). To advance our understanding of the efficacy of psychosocial interventions for caregivers of people with dementia, a more systematic approach is required. Intervention components need to be carefully contrasted in appropriately designed studies of sufficient size.

No evidence exists for methylation inactivation of the p16 tumor suppressor gene in ovarian carcinogenesis.

The p16ink4/CDKN2/MTS1 tumor suppressor gene encodes a cyclin-dependent kinase inhibitor which plays an important role in regulation of the G1/S phase cell cycle checkpoint. Loss of heterozygosity (LOH) at the p16 locus, 9p21, has been documented in a wide variety of tumors including ovarian carcinoma. However, inactivating mutations of the remaining allele and homozygous deletions are relatively infrequent events in primary tumors, even in cases where expression of p16 at the mRNA and protein level is clearly absent. These findings initially cast doubt on the role of p16 as a tumor suppressor gene in vivo. Recently, an alternative mechanism of p16 inactivation involving methylation of the CpG island in the 5' region of the gene has been demonstrated in a number of malignancies and cell lines. In this study we have analyzed the methylation status of four CpG dinucleotides in a panel of 23 ovarian tumors using a multiplex PCR approach to correlate our findings with the LOH data in this region. Using the microsatellite markers D9S171 and D9S1679 LOH was demonstrated in 4/22 (18%) informative cases. All 23 tumors showed no evidence of methylation at the p16 locus including the 4 tumors demonstrating LOH at 9p21. These results suggest that methylation inactivation of the p16 gene does not play an important role in ovarian carcinogenesis.