Background: It is generally believed that the pathogenesis of PINK1/parkin-related Parkinson's disease (PD) is due to a disturbance in mitochondrial quality control. However, recent studies have found that PINK1 and Parkin play a significant role in mitochondrial calcium homeostasis and are involved in the regulation of mitochondria-endoplasmic reticulum contact sites (MERCSs).
Objective: The aim of our study was to perform an in-depth analysis of the role of MERCSs and impaired calcium homeostasis in PINK1/Parkin-linked PD.
Introduction: Thrombolysis has been shown to improve neurological recovery in acute stroke. But the response to thrombolysis is variable across patients. We sought to investigate this variability by analyzing the lesion patterns following systemic thrombolysis with recombinant tissue plasminogen activator (rtPA) and tirofiban in middle cerebral artery (MCA) stroke.
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