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Chronic treatment with A�� drastically reduced synaptic transmission and the extent of secretory vesicles, which were recovered partially with BB-4. Also, the extract recovered Ca2+ transients in hippocampal neurons preincubated with A�� (0.5 and 5 ��M) by about 25% �� 3% and 30% �� 2, respectively. In this work, we demonstrate a novel effect of the BB-4 extract on A��-induced ATP leakage, in which this extract was able to antagonize the acute ATP leakage but not chronic ATP depletion. On the other hand, BB-4 prevented the uncoupling of mitochondrial function induced by FCCP by about 85%, but it was unable to modify the uncoupling induced by A��. The present results strongly indicate that BB-4 plays a role [http://www.selleckchem.com/products/epz-6438.html EPZ-6438 mouse] in the process of A�� aggregation by reducing the toxic species (i.e., 40 kDa). These findings suggest that a blueberry extract can protect neuronal tissue from A�� toxicity mainly through its antiaggregation property, and its antioxidant properties and mitochondrial membrane potential capacities are secondary mechanisms important in chronic stages. Our work suggests that BB-4 could be an important nutritional complement to neuronal health as well as a potential nutraceutical formulation useful as a dietary supplement in the elderly. ? 2011 Wiley-Liss, Inc. ""Treatment with bone marrow stromal cells (BMSCs) ameliorates [http://en.wikipedia.org/wiki/GRB10 GRB10] neurological functional deficits after stroke. Nerve growth factor (NGF) is a neurotrophic factor that supports the survival and growth of neural cells. Noggin, an [http://www.selleckchem.com/products/PD-0325901.html www.selleckchem.com/products/PD-0325901.html] antagonist of bone morphogenetic protein (BMP), promotes the differentiation of stem cells into neurons. In this study, we hypothesize that transfection of NGF and Noggin in BMSC treatment of stroke promotes BMSC neuronal differentiation and improves functional outcome after stroke. Adenovirus was used to trasfect NGF and Noggin and the transfection efficiency was measured by Western blot and immunostaining in vitro. The transfected BMSCs with NGF and/or Noggin were administered intravenously at 5 days after middle cerebral artery occlusion (MCAo) in rats. The neurological functional outcome and BMSC migration and differentiation in the ischemic brain were measured. The transplantation of BMSCs with NGF or Noggin elicited neurological functional improvement, promoted BMSCs present in the ischemic brain, and also up-regulated neuro-like cell differentiation as well as increased synaptophysin expression in the ischemic brain compared with nontreatment control animals (P