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View profile for Sharief Taraman, MD, DABPN, DABPM, FAAP, graphic

CEO, Associate Professor, Pediatric Neurology & Clinical Informatics - Former Division Chief | Innovation, Medical Devices & AI in healthcare

I had the pleasure of recently recording a podcast for Healio with my good friend and colleague Hansa Bhargava MD. One of the topics that came up was what was how did pediatric neurologist like myself got involved with both Cognoa leading the way in #autism #neurodevelopment and #behavioralhealth in #pediatrics but also end up advising Cognito Therapeutics, Inc. with a #breakthrough for treatment for #Alzheimers. You'll have to stay tuned to find out and hear about the overlap between #neurodevelopmental and #neurodegenerativediseases. I'm not the only one though, check out this research out of University of Exeter, Radboud University, UMC Utrecht Brain Center, Utrecht University, Heidelberg University, University of Groningen, & Tokyo University of Science from coauthors Martien Kas, J. Peter H. Burbach, Asami Oguro-Ando, Amila Zuko, et al. revealing protein Contactin-4's (CNTN4) role in neuron development and interaction with protein Amyloid Precursor Protein (APP), impacting both #neurodevelopmentaldisorders and #AlzheimersDisease. My summary: >Cntn4 Knockout Mice Cntn4-deficient mice exhibit reduced cortical thickness in the motor cortex region and altered dendrite length and branching in pyramidal neurons. Overexpression of CNTN4 in primary neurons results in significantly longer dendrites, suggesting CNTN4 promotes neurite outgrowth. >CNTN4-APP Interaction Mass spectrometry analysis identified APP as a binding partner of CNTN4. In CNTN4-/-, APP-/-, and CNTN4-/-/APP-/- knockout cells, total neurite length, longest neurite length, and cell area were significantly reduced compared to control cells. This suggests the CNTN4-APP interaction contributes to their gene expression and neurite outgrowth. >Relevance to Neurodevelopmental Disorders Abnormalities in the motor cortex and neurite outgrowth defects observed in Cntn4-deficient mice align with connectivity and phenotypic abnormalities seen in autism. The findings provide insights into the role of CNTN4 and its interplay with APP in neural development, which may be relevant for understanding the etiology of neurodevelopmental disorders like autism and neurodegenerative disorders like Alzheimer's Disease. Read the full text here: https://lnkd.in/ghWN5eYq

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