Mutations of the PTEN gene cause neurons to grow to twice the size and form four times the number of synaptic connections to other neurons as a normal neuron. Removing the RAPTOR gene, an essential gene in the mTORC1 signaling pathway, prevents the neuronal and synaptic overgrowth associated with PTEN mutations. Using Rapamycin to inhibit mTORC1 recues all the changes in neuronal overgrowth.
Glioblastoma brain cancer originates from a pool of stem cells that can be a significant distance away from where the tumor eventually forms.
An over-production of eIF4E impairs microglial cells, hampering their ability to effectively prune synapses and leading to autism-like behaviors in male mouse models of ASD.
Reducing levels of the Alzheimer's related Tau protein prevents autism-like behaviors in mouse models. Tau reduction also prevented seizures in the animals.
Postmortem study reveals those with ASD have cellular abnormalities that impair the production of myelin.
Copy number variants may act as genetic modifiers that influence the risk of autism and developmental delay versus cancer risk in people with PTEN mutations.
Genetically silencing mTORC2 in mouse models prolonged lifespan, suppressed seizures, increased long-term memory, and reduced autism-like behaviors.
A metabolite has been identified that can predict whether people with PTEN mutations will develop cancer or ASD.
Teriflunomide, a drug commonly used to treat multiple sclerosis, shows promise for the treatment of glioblastoma when coupled with targeted cancer therapies.
PTEN deficiency drives an increased expression of LOX. LOX attracts macrophages which protect gliobastoma brain cancer cells and provide growth factor support for the tumor, a new mouse study reveals.
Researchers will present their latest findings regarding genes associated with autism spectrum disorder in an upcoming meeting.
Targeting the gene WWP1 with indole-3-carbinol, a compound found in broccoli and other cruciferous vegetables, suppressed tumor growth in animal models of cancer.