Open positions:
We are looking for students studying towards
MSc and PhD.
We are also looking for excellent Post-Doctorate candidates for a challenging project.
DEVELOPMENTAL NEUROSIENCE
Hava M. Golan, Ph.D
Research Interest
Our studies focus on the interaction between genetics and the in-utero environment and its impact on brain development.
Genetic and Environmental factors in autism
Mthfr gene and one carbon metabolism in brain development
1. Nutrigenomic intervention strategy to reduce autistic behavior rates – preclinical study in mice.
Individuals with ASD, a variable population whose members are spread along the autism spectrum, include verbal individuals with difficulties in social skills, non-verbal individuals with intellectual disabilities and the vast spectrum between these conditions. These sub-populations differ in their quality of life, needs and levels of dependence on family and societal support. Effective intervention, therefore, should be personalized and adjusted to well-defined subgroups of ASD patients.
Among individuals on the autism spectrum, about 30% or approximately 400,000 children in the US are estimated to suffer from low functioning of one-carbon (C1) metabolism. This condition may be due to genetic variations, feeding habits or gastrointestinal issues. Our study will focus on a way to improve the quality of life of this target population.
We develop a nutrigenomic intervention strategy to reduce risk for ASD and to improve quality of life in a subgroup of ASD patients who suffer from low C1 metabolic activity due either to genetic or to non-genetic causes.
In the short term, our pre-clinical study will provide proof of concept for the benefits of personalized nutritional intervention, including reduced risk for ASD, improved prognosis of affected children, and possible attenuation of ASD symptoms.
We also investigate the changes in the GABA pathway associated with C1 metabolism markers as an additional potential target for drug therapy.
Translating these findings into recommendations for humans will offer a viable, practical means to aid affected children and families and in the process to reduce the load on society.
CaM-KMT gene, intellectual disabilities and brain development
Intellectual disabilities escape diagnostic definition in 75-90% of cases and mitochondrial defects are an increasingly recognized cause of developmental, degenerative and systemic disorders. Patients deleted for the methyl transferase gene in contiguous gene syndromes present severe clinical manifestations including severe intellectual disabilities and mitochondrial disease. In collaboration Prof. Parvari we described the importance of Calmodulin (CaM) methyl-transferase (CaM KMT) in mouse brain. Our previous studies pointed specifically on the importance of CaM methylation since mice deleted for the CaM methyl transferase gene recapitulate these clinical manifestations.
We search for the molecular mechanisms involved in the methylation of CaM: the identification of the pathways depending on the methylation status of CaM and the importance of these pathways in neurogenesis and neuronal and mitochondrial function.
In the long term, given the ubiquitous and highly conserved nature of CaM and CaM KMT, the impact of methylation-mediated regulation at the cellular and molecular levels is expected to provide a transformative contribution to the broad field of Ca++/CaM signaling.
Nutritional intervention in Autism
A talk in the autism forum 5.4.21 (general audience)
