While a late occurrence and larger area of hyperperfusion indicate a large infarct. Vasodilatory capacity can recover in former areas of hyperperfusion and even be above baseline at later time points, AbMole 3,4,5-Trimethoxyphenylacetic acid indicating recovery of vascular function or integration of newly formed blood vessels into the infarct border zone. Three major pathological features are extracellular abnormal deposition of b-amyloid, the formation of senile plaques by glial cell activation, and the formation of neurofibrillar tangles by the aberrant phosphorylation of the intracellular protein Tau. These pathologies result in dysfunction and neuronal loss in the hippocampus and cortex in AD patients. Several previous studies have demonstrated that abnormal formation and deposition of Ab are extremely critical to AD development. Extracellular studies have shown that the fibrillation of Ab promotes the loss and apoptosis of neurons,; however, the underlying mechanism is still unknown. A more recent study has told that Ab derives from amyloid precursor protein. Thus we propose that Ab promotes neurotoxicity, which affects specific neuronal mediators localized to the membrane and their interactions. It has been shown that several receptors and proteins interact with Ab. The integrin family is a class of cellular adhesion molecules with adhesive and signal-transduction functions. They function as heterodimers, which consist of a and b subunits, and bind noncovalently to mediate cell-cell and cell-extracellular matrix interactions. Itgs participate in the regulation of the signaling pathways involved in growth, hypertrophy, survival, differentiation, migration, cell morphology and apoptosis. Growing evidence has demonstrated that Itgs play an important role in AD. Hetero-an antagonists can block the inhibition of long-term potentiation induced by Ab in vivo and in vitro, suggesting that the an Itg is an important regulator of synaptic dysfunction, plasticity diversity and long-term potentiation in the early stages of neurodegenerative diseases. The heterodimers a2b1, a5b1, anb1 and anb3 can facilitate the deposition of Ab and induce neurotoxicity, which results in neuronal loss. However, the mechanism by which AD is mediated by Itgs is still unknown. Our study used cultured primary hippocampal neurons as a model for Ab neurotoxicity. We used the specific antagonists, an and b1, to observe the function of these two Itg subunits during Ab-induced apoptosis. Using siRNA technology, focal adhesion kinase, an important downstream effector of Itgs, was silenced to explore the mechanism of an- and b1-mediated Abinduced neurotoxicity. We found that both 17E6 and ab58524, which are specific antagonists of an and b1, respectively, inhibited the apoptosis of hippocampal neurons induced by Ab, indicating a potential link with the activation of the Itg-FAK signaling pathway. The Ab hypothesis has been widely studied and supported by many studies in the pathogenesis of AD.