Paramita Chakrabarty

Eg5 (kinesin-5) has emerged as a critical therapeutic target in cancer treatment, particularly for aggressive and rapidly dividing tumors. This microtubule-based motor protein is essential for the formation and function of the mitotic spindle, facilitating centrosome separation and bipolar spindle assembly during cell division.1 These processes are crucial for accurate chromosome segregation and mitotic progression.

Main text (Neuron 87, 963–975; September 2, 2015) We have become aware of errors in two figure panels (Figures 6B and 6E) in our paper. In the original Figure 6B, the NeuN image of the “Appoptosin + C3I” group was mispresented due to an unintentional copy-paste error. In Figure 6E, incorrect images for the NeuN and GFAP were used for the “Tau KO Control” group. These errors occurred during the assembly of the figure panels.

Abstract Background: Exposure to repetitive head impacts (RHI) is associated with increased risk for chronic traumatic encephalopathy (CTE), a neurodegenerative tauopathy, and other neuropathological changes. Biological drivers of RHI-related neurodegeneration are not well understood. We interrogated the plasma proteome in aging adults with prior RHI compared to healthy controls (CTL) and individuals with Alzheimer's disease (AD), including a subset characterized neuropathologically at autopsy.