Grants awarded through this request for applications are intended to advance the understanding of autism spectrum disorder through analyses of human postmortem brain tissue donated to the Autism BrainNet collection.
The annual budget is between $300,000 and $1,000,000, inclusive of 20 percent indirect costs, for a period of two (2) years.
We encourage proposals from multiple investigators only when such collaborations are well justified by the expected benefits to the proposal. For collaborative proposals, the annual budget can exceed the project cap stated above but should not exceed a total of $2,000,000 inclusive of 20 percent indirect costs.
Simon Chen and colleagues found that a reduction in locus-coeruleus noradrenaline neuromodulatory signaling contributes to altered motor learning in 16p11.2 deletion mice.
Tesar joined the faculty at CWRU in 2010 and is currently the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics at CWRU School of Medicine. His laboratory has pioneered new regenerative approaches to treat myelin disorders of the central nervous system, including multiple sclerosis, neuromyelitis optica, pediatric leukodystrophies, cerebral palsy and brain cancer.
Emmanuel Mignot discussed sleep biology as well as sleep disorders and their impact. He presented a link to what is known on the genetics of sleep and sleep disorders. He emphasized the need for large scale objective sleep recording studies with genomic and proteomic analysis to better understand the molecular pathways regulating sleep and circadian biology.
The mitochondrial genome encodes genes critical for energy production within the brain. Many lines of
evidence suggest that mitochondrial function may be impaired in autism. Neal Sondheimer will evaluate the
association between mitochondrial mutations and their interactions with the nuclear genome and the risk
for autism.
Neuronal activity triggers the expression of new genes that play a critical role in aspects of neural development and cognitive function. Building on evidence suggesting links between a class of ASD susceptibility loci (i.e., subunits of the BAF chromatin remodeling complex) and this form of gene regulation, Michael Greenberg and colleagues seek to determine whether disruption in neuronal activity-responsive chromatin remodeling underlies the effects of these ASD mutations.
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