Professor Peter Kind is Director of the Patrick Wild Centre and Simons Initiative for the Developing Brain (SIDB) for Research into Autism, Fragile X Syndrome (FXS) and Intellectual Disability and Professor of Developmental Neuroscience at the University of Edinburgh. He is also Associate Director at the Centre for Brain Development and Repair (CBDR) at the Institute for Stem Cell Biology and Regenerative Medicine (Instem), Bangalore, India.

Professor Kind completed his postdoctoral training with Professor Colin Blakemore at Oxford University and Professor Susan Hockfield at Yale University. Professor Kind received his PhD from Oxford University in 1993. 

Email: P.Kind@ed.ac.uk 

The Kind lab aims to understand the neurological basis of monogenic forms of autism and intellectual disability, such as fragile X syndrome (FXS), SYNGAP1 haploinsufficiency and CDKL5 deficiency disorder (CDD). 

Our research is designed to address two key questions: 

1. Do developmental disorders have critical periods for treatment?   

For decades it was believed that the adult brain was hard-wired, and that interventions for  neurodevelopmental disorders (of which autism is a component), would be most effective if implemented during the first few years of life. This dogma has recently been questioned for several monogenic forms of autism with intellectual disability. To determine whether there are critical periods for therapeutic intervention, we employ proof-of-concept genetic and pharmaceutical rescue studies to determine the effectiveness of potential therapies. By employing a systematic approach to reversibility, as well as identifying developmental trajectories for the appearance of cellular, circuit and cognitive deficits, we address fundamental questions about the extent to which these neurodevelopmental disorders can be treated throughout the lifespan.  

2. Does genetic heterogeneity mask underlying convergence onto a common developmental pathophysiology?    

Of the many genes that have been causally-linked to autism, many cluster around common cellular processes including synaptic function and epigenetic regulation. This genetic convergence raises the possibility of common therapeutic avenues for diverse genetic causes. We examine whether different genetic models of autism display recurrent cellular, circuit and/or behavioural phenotypes that respond to common treatment strategies. Our recent studies suggest many of the cellular phenotypes observed in our models reflect homeostatic or compensatory changes in neuronal function. These compensatory changes serve to lessen the cellular and circuit effects of genetic mutations and could explain, in part, apparent physiological and behavioural convergence between models.