The beneficial effects on cardiovascular disease and related mortality including various risk factors for cardiovascular disease (particularly lowering circulating triglyceride levels and the triglyceride:HDL-cholesterol ratio) have been observed in the absence of any concomitant blood cholesterol lowering. With appropriate dosages, consistent reductions in both fasting and postprandial triglyceride levels and moderate increases in fasting HDL-cholesterol levels have been observed

with algal DHA in the majority click here of trials. These results are similar to findings for fish oils containing DHA and EPA. Related to greater fish intake, higher levels of DHA in circulating blood biomarkers (such as serum phospholipid) have been associated with reduced risks for the progression of coronary atherosclerosis and lowered risk from sudden cardiac

death. Controlled clinical trials have also indicated the potential for algal DHA supplementation to have moderate beneficial effects on other cardiovascular disease risk factors including blood pressures and resting heart rates. Recommended intakes find more of DHA+EPA from numerous international groups for the prevention and management of cardiovascular disease have been forthcoming, although most have not offered specific recommendations for the optimal individual intake of DHA and EPA. (C) 2009 Elsevier Ltd. All rights reserved.”
“Animal models that make use of chemical toxins to adversely affect the nigrostriatal Mdivi1 cell line dopaminergic pathway of rodents and primates have contributed significantly towards the development of symptomatic therapies for Parkinson’s disease (PD) patients. Although their use in developing neuro-therapeutic and -regenerative compounds remains to be ascertained, toxin-based mammalian and a range of non-mammalian models of PD are important tools in the identification and validation of candidate biomarkers for earlier diagnosis, as well as in the development of novel treatments that are currently working their way into the clinic. Toxin models of PD have and continue

to be important models to use for understanding the consequences of nigrostriatal dopamine cell loss. Functional assessment of these models is also a critical component for eventual translational success. Sensitive behavioural testing regimens for assessing the extent of dysfunction exhibited in the toxin models, the degree of protection or improvement afforded by potential treatment modalities, and the correlation of these findings with what is observed clinically in PD patients, ultimately determines whether a potential treatment moves to clinical trials. Here, we review existing published work that describes the use of such behavioural outcome measures associated with toxin models of parkinsonism.