Gene therapy targets interneurons to tackle Dravet syndrome
The approach, tested in mice, selectively boosts the expression of the autism-linked gene SCN1A in a subgroup of inhibitory cells.
The approach, tested in mice, selectively boosts the expression of the autism-linked gene SCN1A in a subgroup of inhibitory cells.
ADNP and SHANK3 proteins may bind together and alter a neuron’s internal scaffold, hinting at a mechanism that, when disrupted, may underlie several forms of autism.
Of nine genetic models examined in a new study, all had some incidence of cardiac abnormalities. But the problems varied widely depending on the affected genes.
Animals with different autism-linked mutations share disruptions to the mTOR signaling pathway, pointing to a potential molecular mechanism for the atypical cerebellar development seen in some autistic people.
The young researcher from Uruguay uses her expertise in genetics — and discipline as a former athlete — to untangle sleep’s role in neurodevelopmental conditions, one experiment at a time.
Ramping up levels of one isoform of the autism-linked protein reverses traits in model mice, a new study shows.
A new study is the first to link social, repetitive and motor behaviors to mutations in BMAL1, which regulates the body’s circadian rhythms.
Interneurons that fail to propagate electrical signals in mice that model Dravet syndrome may cause the animals, like people with the autism-linked condition, to die suddenly.
The experimental compound, called GSK-LSD1, enhances social preferences and reduces repetitive grooming in mice, according to a new study.
Together, the neurons are part of the corticostriatal circuit, which has been implicated in autism.