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Accordingly, it has been proposed that AD is an angiogenesis-dependent disorder and that the development of anti-angiogenic drugs acting on abnormal intravascular brain endothelial cells may be able to prevent and treat AD (Vagnucci and Li 2003)

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For example, PINK1 and Parkin loss of function impair mitophagy and cause accumulation of damaged mitochondria, leading to enhanced electron leakage and formation of superoxides 11,12,13

In contrast, the Ischemia-Reperfusion group showed increased fluorescence intensity, indicating the accumulation of nanoparticles

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