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SHANK3

·July 26, 2019·3 min read

Brain region linked to altered social interactions in autism model

The anterior cingulate cortex (ACC) plays a critical role in regulating social behaviors. In mouse models of ASD, dysfunction in the ACC was linked to social impairments associated with the disorder.

Featured Genetics Neuroscience

·June 12, 2019·7 min read

Using gene editing, neuroscientists develop a new model for autism

Using CRISPR gene editing, researchers introduce the SHANK3 gene variant into macaque monkeys. SHANK3 has previously been linked to autism in humans. The monkeys with the SHANK3 mutations exhibited behavioral traits and brain activity patterns similar to those seen in humans on the autism spectrum, Researchers hope the new model will facilitate new avenues of research for ASD.

These are fmri scans of the female mice brains lacking shank3

Autism Featured Genetics Neuroscience

·May 7, 2019·2 min read

Autism gene linked to brain and behavior deficits in mice

A deficiency of the SHANK3 gene, a gene associated with ASD, results in structural and functional deficits in the prefrontal cortex. The functional and structural alterations in the PFC were linked to an impairment in social interaction in male mice.

This showa a child looking at a DNA strand

Autism Featured Genetics Neuroscience Open Neuroscience Articles

·April 29, 2019·5 min read

Study links gene to sleep problems in autism

Deficiencies in the SHANK3 gene have been linked to sleep disruptions in both mouse models and people with ASD. Researchers found patients with Phelan-McDermid syndrome, a genetic disorder associated with autism, report trouble falling, and staying asleep. In mouse models, animals lacking the SHANK3 gene had a reduction in deep sleep quality and spent more time awake when other mice were sleeping.

Autism Featured Neuroscience Open Neuroscience Articles

·November 9, 2018·4 min read

Autism Associated with Zinc Deficiency in Early Development

A new study reveals a mechanistic link between zinc levels in fetal development, genes and abnormal neural connections associated with autism.

Autism Featured Genetics

·February 16, 2018·5 min read

Lab Grown Human Cerebellar Cells Yield Clues to Autism

Researchers have derived purkinje cells from patients with TSC, a genetic syndrome that includes some ASD-like symptoms. The cells, researchers say, have several characteristics that could help explain how ASD develops at the molecular level.

Autism Featured Genetics

·August 18, 2017·3 min read

CRISPR Advances Autism Research

Using CRISPR gene editing technology, researchers target the Shank3 gene in monkey embryos. Research backs previous findings of the importance of the Shank3 gene for brain development and its role in autism.

Autism Featured Neurology Pain

·December 1, 2016·5 min read

Autism Linked Protein Crucial For Feeling Pain

TRPV1 and SHANK3 could play a role in pain insensitivity in people with autism, a new study reports.

Autism Featured Genetics

·September 1, 2016·5 min read

Zinc May Help Reverse Brain Changes in Autism

According to researchers, cellular changes in the brain caused by genetic mutations associated with Autism can be reversed with the help of zinc.

Autism Featured Genetics

·May 25, 2016·4 min read

Illuminating the Role of Autism Linked Shank Gene

A new study reports a gene mutation linked to autism also plays a critical role when it comes to the formation and maturation of synapses.

Autism Featured Genetics Neuroscience Videos Open Neuroscience Articles Psychology

·May 10, 2016·5 min read

Mouse Model of Autism Offers Insights For Human Patients

Researchers have developed a new mouse model of a genetically linked type of autism. The new model helps reveal more about the role of genes and brain changes associated with the disorder.

Autism Featured Genetics

·February 18, 2016·5 min read

Researchers Reverse Autism Symptoms

Researchers demonstrate they can reverse some autism symptoms in mice by turning the Shank3 gene on later in life, allowing the brain to correctly rewire itself.