Charting the structure and function of the brain’s many circuits may unravel autism’s mysteries.
Clues that problems with mitochondria contribute to autism have been accumulating for decades. In the past five years, a mutant mouse and a flurry of findings have energized the field.
Model mice of the subtype also show hyperactivity in a signaling pathway called mTOR, bolstering the idea that distinct forms of autism have different biological roots and may require different treatment approaches.
An atypical thalamus may underlie not only sensory issues in autism but also difficulties with social skills, attention and memory.
Cortical organoids that contain non-neuronal brain cells called microglia may reflect human neurodevelopment more faithfully than those that don’t.
The work fills in gaps about how synapses change before and after birth — essential knowledge for understanding whether synapse development differs in autism.
These short reports from Spectrum journalists highlight some of the autism-related findings that caught our attention at the meeting this past week.
Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.
Animal models of autism rooted in exposure to maternal antibodies hint at different mechanisms.
Dysfunctional circuits and a rogue sodium channel in the brainstem may explain the disordered breathing pattern seen in children with Pitt-Hopkins syndrome, a form of autism.
Audrey Brumback riffs about volunteering in Mexico, having a lab next door to her husband’s and why she sometimes cries at work.
