In a keynote lecture on Tuesday at the Society for Neuroscience annual meeting in San Diego, Nat Heintz predicted that over the next ten years, scientists will piece together detailed molecular signatures of each of the hundreds of cell types in the mouse brain. After the talk, he sat down with SFARI on a sunny patio to discuss what this decade of advancements might mean for autism research.
The brains of people with autism have abnormally dense and stubby dendritic spines, the neuronal projections that receive electrical signals, according to data presented Monday at the Society for Neuroscience annual meeting in San Diego.
If you give most mice a choice between sniffing a new playmate and a new object, most will choose the new playmate every time. But not BTBR or SHANK3 mutant mice, which spend less time engaging in social interactions with other mice. Does that mean these mice have autism?
Mice missing a large protein at the junction between neurons show motor impairments, anxiety and increased social behaviors, according to a study in the American Journal of Psychiatry. The protein, postsynaptic density-95 or PSD-95, is part of a key molecular bridge connecting other proteins linked to autism.
SHANK1 — a member of a family of proteins linked to autism — does not cause autism-like social deficits when mutated in mice, according to a study published online in September in Brain Research.
Researchers have uncovered an important molecular piece of a learning mechanism that occurs at the junction between neurons. The findings, which may help understand how the brain is disrupted in disorders such as autism, appear in the 24 June issue of Neuron.
Several independent groups have found previously unknown risk genes for autism, schizophrenia and mental retardation. The candidate genes have one thing in common: they encode proteins that are needed for the healthy function of synapses, the junctions between neurons.
A chilling new technique shows the intricate and coordinated activity of previously mysterious pieces of the synapse, the all-important junction between neurons that allows cells to talk to each other.
Although the head overall is bigger in some children with autism, researchers have found more informative differences in size — some smaller, some larger — across regions of the brain.
Mice lacking a gene located in the chromosomal region 22q13 — which has been linked to autism — have motor learning and social deficits reminiscent of the disorder, according to unpublished findings presented in a poster session yesterday at the Society for Neuroscience meeting in Chicago.