Potential antifilarial activity of the fruit, leaf and stem extracts of Melia azedarach Linn. on cattle filarial parasite Setaria cervi in vitro

The effect of aqueous and alcoholic extracts of the fruit, leaf and stem of Melia azedarach Linn.(Meliaceae) on the spontaneous movements of both the whole worm and the nerve-muscle(n.m.) preparation of Setaria (S.) cervi and on the survival of microfilariae in vitro was studied.Alcoholic extracts of fruit, leaf and stem caused inhibition of the spontaneous movements of thewhole worm and the n.m. preparation of S. cervi, while only aqueous extract of fruit causedinhibition of the spontaneous movements of the whole worm and the n.m. preparation of S.cervi. The initial stimulatory effect was not observed by the aqueous and alcoholic extracts offruit on n.m. preparation. The concentrations required to inhibit the movements of the wholeworm and n.m. preparation for alcoholic extracts of fruit, leaf and stem were 250, 40 µg/ml;280, 40 µg/ml and 270, 25 µg/ml respectively, whereas an aqueous extract of fruit causedinhibition of whole worm and n.m. preparation at 200 µg/ml and 40 µg/ml respectively.Alcoholic extracts of the fruit, leaf and stem and aqueous extract of the fruit of M. azedarachcaused concentration related inhibition on the survival of microfilariae (m.f.) of S. cervi. TheLC50 and LC90 as observed after 6 h were found to be 5, 15, 10, 20 ng/ml and 10, 25, 20 and 35ng/ml, respectively. This work was conducted in view of the exploration of potentialantifilarial herbal drug

Does physical activity reduce risk for Alzheimer’s disease through interaction with the stress neuroendocrine system?

Lack of physical activity (PA) is a risk factor for Alzheimer's disease (AD) and PA interventions are believed to provide an effective non-pharmacological approach for attenuating the symptoms of this disease. However, the mechanism of action of these positive effects is currently unknown. It is possible that the benefits may be at least partially mediated by effects on the neuroendocrine stress system. Chronic stress can lead to dysfunction of the hypothalamic pituitary adrenal (HPA) axis, leading to aberrant basal and circadian patterns of cortisol secretion and a cascade of negative downstream events. These factors have been linked not only to reduced cognitive function in the non-demented but also increased levels of Amyloid β plaques and protein Tau "tangles" (the neuropathological hallmarks of AD) in mouse models of this disease. However, there is evidence that PA can have restorative effects on the stress neuroendocrine system and related risk factors relevant to AD. We explore the possibility that PA can positively impact upon AD by restoring normative HPA axis function, with consequent downstream effects upon underlying neuropathology and associated cognitive function. We conclude with suggestions for future research to test this hypothesis in patients with AD