Alzheimer's disease (AD) is a prevalent and debilitating neurodegenerative disease that leads to substantial loss of quality of life. Therapies currently available for AD do not modify the disease course and have limited efficacy in symptom control. As such, novel and precise therapies tailored to individual patients' neurophysiologic profiles are needed.
View Article and Find Full Text PDFMajor depressive disorder (MDD) is a prevalent and debilitating psychiatric disease that leads to substantial loss of quality of life. There has been little progress in developing new MDD therapeutics due to a poor understanding of disease heterogeneity and individuals' responses to treatments. Electroencephalography (EEG) is poised to improve this, owing to the ease of large-scale data collection and the advancement of computational methods to address artifacts.
View Article and Find Full Text PDFThe Wnt/β-catenin signaling governs anterior-posterior neural patterning during development. Current human pluripotent stem cell (hPSC) differentiation protocols use a GSK3 inhibitor to activate Wnt signaling to promote posterior neural fate specification. However, GSK3 is a pleiotropic kinase involved in multiple signaling pathways and, as GSK3 inhibition occurs downstream in the signaling cascade, it bypasses potential opportunities for achieving specificity or regulation at the receptor level.
View Article and Find Full Text PDFWith a wide variety of dopamine transporter (DAT) antibodies available commercially, it is important to validate which antibodies provide sufficient immunodetection for reproducibility purpose and for accurate analysis of DAT levels and/or location. Commercially available DAT antibodies that are commonly used were tested in western blotting (WB) on wild-type (WT) and DAT-knock-out (DAT-KO) brain tissue and with immunohistology (IH) techniques against coronal slices of unilaterally lesioned 6-OHDA rats, in addition to wild-type and DAT-knock-out mice. DAT-KO mice and unilateral 6-OHDA lesions in rats were used as a negative control for DAT antibody specificity.
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