Fisheries co-management : ecological and social impacts. A case study of Northern Mozambique

Co-management, or participative management of fisheries, consists of returning or opening to the community the management of fisheries. This work, carried out in northern Mozambique, analyzed the ecological and social impacts of the implementation of co-management of fisheries. Firstly 198 species of fish were found and photographed and a guide to identification of species - essential to who works in the marine environment – was produced. Following, the spill-over effect was identified in a marine sanctuary. It occurred after 6 years and only for herbivore fishes and not to the carnivores. In order to evaluate co–management of fisheries effects, the captures of the entire province were analyzed. No differences were found in the diversity of the species caught, but an increase of the fish size was detected: this size was smaller in the fishing centers with no CCP (Community Fishing Councils), slightly bigger in the fishing centers with CCP and even bigger in the fishing centers with a more efficient management. At the same time it was observed that the size of the fish caught is bigger in the fishing centers further away from the markets. In addition to the ecological effects and the effects on fisheries, it was also analyzed the point of view of those who live the co-management. The socioeconomic factors that have a stronger influence in their perceptions are the age and the wealth. Finally and according to the CCP members, their main achievements are in the fisheries inspection and in the creation of conservation areas. Their main difficulties are the lack of means of transportation and the lack of recognition of the CCP's authority; both among the population and in the coordination with local authorities. This thesis pioneered in Mozambique in assessing the effects of Community sanctuaries and the effects of CCP on fisheries as well as by revealing the profile of the supporters of co-management and marine sanctuaries. Finally, an assessment of the matter of fact problems that the communities have to face when implementing co-management was also made.

The role of cellular prion protein in Alzheimer’s disease

Alzheimer’s disease (AD) is the most prevalent age-related neurodegenerative disease that leads to cognitive impairment and dementia. The major defined pathological hallmark of AD is the accumulation of amyloid beta (Aβ), a neurotoxic peptide, derived from beta and gamma-secretase cleavage of the amyloid precursor protein (APP). It has been described that cellular prion protein (PrPC) plays a role in the pathogenesis of Alzheimer disease. Although, the role of PrPC is still unclear, previous studies showed contradictious results. To elucidate this issue, the main objective of the present study is to investigate the influence of a knockout of the PRNP gene in 5XFAD mice, 5xFAD mice exhibited 5 mutations related to familial Alzheimer disease. These mice show an Aβ1-42 accumulation and an increased neuronal loss during aging. To create a bi-transgenic 5xFAD mice were crossed with Prnp0/0 Zurich 1 mice (prion protein knockout mice). We subjected two transgenic mice (5xFAD and Prnp0/05xFAD) at different ages (3, 9 and 12 months of age) to a battery of task to evaluate cognitive and motoric deficits and a biochemical analysis (ELISA, western blot and immunohistochemistry) to investigate the regulation and potential involvement of downstream signaling proteins in the Aβ induced toxicity process dependent of the PrPC concentration. The study revealed that the deficits induced by Aβ mediated toxicity appeared earlier in 5xFAD mice (9 months of age) than in Prnp0/05xFAD (12 months of age). Investigating the amount of amyloid beta in 5xFAD mice we observed a PrPC dependent regulation in 9 month-old animals of Aβ1−40 but not of the toxic form Aβ1−42. We did not found in Prnp0/05xFAD mice the up-regulation of P-Fyn, Fyn or Cav-1 as we found in 5xFAD mice. This suggests an important role of PrPC in Alzheimer’s disease as a promoter of toxic effect of Aβ oligomers. Our results may suggest the loss of PrPC delays the toxicity of amyloid beta. In conclusion, our data support a role of PrPC as a mediator of Aβ toxicity in AD by promoting early onset of disease.