A Participatory Group Process within a Health Collaborative to Collect and Disseminate Needs Assessment Data.

BACKGROUND: Inclusion of community-based participatory research (CBPR) principles within an epidemiological study design is anticipated to promote the effective integration of knowledge derived from research data collection into the strategic planning and collaborative effort of a group focused on improving community-based health outcomes. This article describes how CBPR principles were used throughout survey design, data collection, analyses and results dissemination. METHODS: A health needs assessment survey was developed as a partnership between an academic research group from the Virginia Commonwealth University (VCU), a neighborhood-level health and wellness collaborative, and community residents. Survey development, pilot testing, data collection, results dissemination, and action among the health collaborative members were carried out using CBPR principles. Feedback from participants at each stage was collected to improve the overall process of data use within the collaborative. RESULTS: Data from 1,064 adult participants living in the East End of Richmond, Virginia, were collected. The use of CBPR and epidemiological approaches was successful in promoting effective collaborative efforts, as indicated by 1) sustained organization-level partner participation in the development of survey items and donation of participant incentives; 2) positive feedback from resident- and organization-level participants in a preliminary data dissemination event; 3) strong resident participation at community-wide dissemination events; 4) increases in survey-related blog traffic occurring in conjunction with community-wide dissemination events; and 5) the use of process protocols and results within similar collaboratives across the city. CONCLUSIONS: Use of CBPR principles with epidemiological methods is a powerful tool for facilitating effective community-level strategic planning within health collaboratives.

Cerebral mitochondrial electron transport chain dysfunction in multiple system atrophy and Parkinson's disease.

Multiple system atrophy (MSA) is a neurodegenerative disease characterised by glial cytoplasmic inclusions (GCIs), containing α-synuclein. Mutated COQ2, encoding an enzyme essential for co-enzyme Q10 (CoQ10) biosynthesis, has been associated with MSA. CoQ10 is an electron carrier in the mitochondrial electron transport chain (ETC) and antioxidant. It has been shown to be deficient in MSA brain tissue, thus implicating mitochondrial dysfunction in MSA. To investigate mitochondrial dysfunction in MSA further we examined ETC activity in MSA and control brain tissue, compared with Parkinson's disease (PD) where mitochondrial dysfunction is known to be important. Using cerebellar and occipital white matter ETC complex I, II/III and IV activities were measured spectrophotometrically, selected individual components of the ETC were assessed by immunoblotting and cellular complex IV activity was analysed by enzyme histochemistry. We show decreased complex II/III activity with increased complex I and IV activity in MSA cerebellar white matter. This corresponds with the deficit in CoQ10 previously described in MSA and reflects the high regional pathological burden of GCIs. This study highlights mitochondrial dysfunction in MSA pathogenesis, suggests an influence on selective regional vulnerability to disease and points to shared disease mechanisms in α-synucleinopathies.