Autism’s ties to the cell skeleton
Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.
Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.
Altered expression of TSC2 and the mTOR pathway reshape the formation of certain synapses between inhibitory and excitatory neurons in mice.
The circuit linking the prefrontal cortex and part of the thalamus is impaired in mice raised in social isolation and in mice with mutations in the FMR1 or TSC2 genes.
Sleep problems may contribute to or derive from autism traits — or both. After decades of work, researchers are beginning to uncover the biological connections between the two conditions, revealing new paths to potential treatments.
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.
Mock viral infections impair social memory in mice with a mutation tied to autism, and autistic boys are more likely than their non-autistic peers to have had serious infections early in life.
Neuronal axons ignore guidance cues after a mutation in the gene TSC2 disrupts signaling through RhoA, a protein regulated by many autism-linked genes.
The overproduction of proteins in brain cells called microglia causes social impairments, cognitive deficits and repetitive behavior in male mice, a new study has found.
Tuberous sclerosis provides a unique opportunity to understand autism because about half of people with that single-gene condition also have autism.
A drug that treats tumors and epilepsy in people with tuberous sclerosis complex does not boost their intelligence or ease autism traits.