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Abstract Atypical sensory processing in neurodevelopmental disorders contributes to cognitive, social, and behavioural disruptions, yet underlying neurophysiological mechanisms remain unclear. Using a mouse model of SYNGAP1 haploinsufficiency (HET), a common monogenic cause of intellectual disability and autism, we investigated visual processing deficits.
History has many definitions. One view is that every history worth the name is a mass of biographies brought together by a single event – or, in the case of military history, a campaign. What writer Damien Wright has done in detailing how a posse of Anzacs went to war again after the 1918 Armistice – is compile 12 chapters of epic daring by multiple protagonists across the world’s biggest land mass.
INTRODUCTION SYNGAP1-related intellectual disability (hereafter SYNGAP1-ID) is a neurodevelopmental disorder caused by pathological variation of the SYNGAP1 gene. Truncating mutations are the most commonly reported in the literature, though others including missense and microdeletions have also been described (Berryer et al., 2013).
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