Carriers of the combined risk genotype had increased frequency of IGT or T2D. The present results have not been replicated and, given the experience of complex trait genetics, warrant caution in interpretation. Mitochondria used to be considered as the primary source of muscle free radicals. This view is now questioned. Nevertheless, mitochondria remain an important location of reactive oxygen species production in contracting muscle. The underlying mechanisms whereby zinc is involved in delayed neuronal death and the neuroprotective effects of CQ after ischemic insult are still obscure. In a hippocampal slice model with oxygen-glucose deprivation, zinc rapidly enters neurons, accumulates in mitochondria, and contributes to consequent mitochondrial dysfunction and cell death, suggesting caspase-dependent neuronal apoptosis after a toxic zinc insult. In the present study, we measured the expression levels of caspase-3 and caspase-9, two key molecules in the caspase-dependent apoptotic cascade, in the ischemic gerbil hippocampus. Our results showed that ischemic insult markedly increased the number of both caspase-3- and caspase-9-positive neurons in the hippocampal CA1 region 3 days after global ischemia. Together with our TSQ and AMG data and previous reports that increased zinc accumulation in the CA1 neurons was observed after transient cerebral ischemia, it is reasonable to speculate that the ischemia-induced zinc rise may trigger the activity of caspases in the CA1 neurons and, consequently, lead to neuronal death. In addition, our data also showed that transient ischemia resulted in an increased level of AIF, a pro-apoptotic mitochondrial molecule and the key factor in the caspase-independent apoptosis signaling pathway. This indicates that ischemia-induced zinc accumulation plays a role in modulating caspase-independent neuronal death following transient cerebral ischemia. In the present study, we further assessed the effects of CQ on modulating the caspasedependent and -independent death pathways in the hippocampus of the ischemic gerbil. Our data showed that administration of CQ significantly reduced the expression levels of caspase-3, -9, as well as AIF in the hippocampus, 3 days after ischemia in the gerbil. Amyloid fibrils are often localized in close proximity to basement membranes, a specialized component of the extracellular matrix that is mainly built of collagen and glycosaminoglycans. GAGs are long unbranched polysaccharides that often occur as O- or N- linked side chains of proteoglycans, with the exception of hyaluronic acid existing in a free form. Tubulin Acetylation Inducer Naturally occurring GAGs include heparin, heparan sulfate, dermatan sulfate, keratan sulfate, chondroitin sulfate and hyaluronic acid. Other non-physiological derivatives of natural GAGs have been used for studies in vitro, such as fully-O-desulfated heparin and dextran sulfate.