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.
We’re tracking tweets that highlight, among other things, the futility of ‘data availability statements’ and some possible fixes, plus visions of a peer reviewer dust-up.
The cells’ altered proliferation rates hint at ways to diagnose and potentially treat autism earlier.
In this edition, researchers sink a purported link between cerebellar volume and autism and buoy a theory about measuring social behaviors.
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.
By as early as age 2, autistic children appear to have a smaller salience network and a larger default mode network, among other differences, than children without the condition.
Neurons with a faulty copy of SETD1A, a gene tied to autism and schizophrenia, show structural abnormalities and altered connectivity patterns.
On Twitter this week, many researchers toasted the geneticists who won the 2022 Kavli Prize in neuroscience, and others offered helpful reminders for the field.
Different combinations of common, rare, inherited and spontaneous mutations may explain why traits vary so widely among autistic people.
Strategies to replace or compensate for mutated copies of the TCF4 gene could lead to treatments for this profound form of autism, a new study suggests.