Head size parts autism into two major subtypes
An imbalance in the number of excitatory neurons in early brain development may account for the difference.
An imbalance in the number of excitatory neurons in early brain development may account for the difference.
The findings in rhesus macaque monkeys may provide clues to sex differences in the heredity of social behavior in people.
Children with congenital heart disease have an increased likelihood of autism. Why?
Experiments offer clues to why certain mutations are associated with autism in some people and not others.
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.