Chromatin remodeling tied to altered splicing in autism model
Exposing neurons to valproic acid, a well-known environmental risk factor for autism, disrupts their ability to generate different proteins from the same gene.
Exposing neurons to valproic acid, a well-known environmental risk factor for autism, disrupts their ability to generate different proteins from the same gene.
The gene, linked to a little-known condition called Weiss-Kruszka syndrome, prevents embryonic stem cells from deviating from their neuronal destiny.
An analysis of 11 cortical regions shows anterior-to-posterior shifts in gene expression linked to autism.
Common variants in five regions of the genome may determine whether someone has one condition versus the other.
A 341-repeat mutation from a person with fragile X does not lead to the syndrome’s traits or function the same way in mice, highlighting a need for different animal models.
Neurons with a faulty copy of SETD1A, a gene tied to autism and schizophrenia, show structural abnormalities and altered connectivity patterns.
Scientists have at last filled in the missing gaps — an advance likely to inform every aspect of autism genetics research, Eichler says.
The experimental compound, called GSK-LSD1, enhances social preferences and reduces repetitive grooming in mice, according to a new study.
The gene, dubbed NHIP, is in a chromosomal region that shows unusually low levels of DNA methylation in placentas from women who gave birth to autistic children.
Inspired by watching her autistic nephew grow up, Croen has also been an advocate for bolstering research and services for autistic adults.