impact of austerity, a “blame culture” and fewer opportunities to work directly with service users
We are often quick to make judgements on what we perceive to be happening when children behave in a way that draws attention – but when a young person with autism is struggling to cope with the world, the last thing they need is our criticism.
These 10 tips reflect our combined experience of research and close engagement with children with autism. And as a proud parent of a boy with autism, I would like everyone to think more about how they respond to children.
Because if we take time to respect and understand people with autism our communities will become more enriching and inclusive for everyone.
1. See me for who I am
Disabled activists have welcomed “timely” new research that concludes that the government’s “fitness for work” process has caused a deterioration in many people’s mental health which they have failed to recover from, and has even led to thoughts of suicide.
The research, Mental Health And Unemployment In Scotland, was carried out by academics at Scotland’s Heriot-Watt and Edinburgh Napier universities*.
Researchers spoke in-depth to 30 people across Scotland with mental health conditions who had experienced the work capability assessment (WCA) system, as well as staff from advice and advocacy organisations.
They concluded that the assessors, employed by the US outsourcing company Maximus, “do not appear to have appropriate expertise in mental health”.
And they added: “The WCA experience for many, caused a deterioration in people’s mental health which individuals did not recover from.
“In the worst cases, the WCA experience led to thoughts of suicide.”
Professor Abigail Marks, one of the report’s authors, said their research showed that WCAs were “fundamentally discriminatory to people with mental health conditions”.
The research emerged as disabled people’s organisations gave evidence this week to the UN’s committee on the rights of persons with disabilities about the UK government’s failure to implement the UN disability convention.
New method uses biochemistry to accurately predict whether a child will develop autism spectrum disorder by measuring the products of metabolic processes.
Researchers at Beth Israel Deaconess Medical Center (BIDMC) have gained new insight into the genetic and neuronal circuit mechanisms that may contribute to impaired sociability in some forms of Autism Spectrum Disorder. Led by Matthew P. Anderson, MD, PhD, Director of Neuropathology at BIDMC, the scientists determined how a gene linked to one common form of autism works in a specific population of brain cells to impair sociability. The research, published in the journal Nature, reveals the neurobiological control of sociability and could represent important first steps toward interventions for patients with autism.
Anderson and colleagues focused on the gene UBE3A, multiple copies of which causes a form of autism in humans (called isodicentric chromosome 15q).Conversely, the lack of this same gene in humans leads to a developmental disorder called Angelman’s syndrome, characterized by increased sociability. In previous work, Anderson’s team demonstrated that mice engineered with extra copies of the UBE3A gene show impaired sociability, as well as heightened repetitive self-grooming and reduced vocalizations with other mice.
Fragile X syndrome is the most common cause of autism. Even though the single gene that’s responsible for it was discovered in 1991, and the disease is detected by a simple blood test, there’s no treatment or cure.
A team of researchers led by Michigan State University, however, has provided a promising lead in battling this disease. In the current issue of Nature Communications, the scientists identified a single protein that appears to be the culprit in causing many behavioral symptoms as well as molecular and cellular abnormalities related to Fragile X.
“We began with 600-800 potential protein targets, searching for the equivalent of a needle in a haystack,” said Hongbing Wang, MSU physiologist and study co-author. “Our needle turned out to be ADCY1. When we compared levels of this protein in Fragile X mouse model to normal controls, we saw a 20-25 percent increase of ADCY1.”
Subsequent tests of the team’s prime-target protein on the Fragile X mouse model revealed four key results. First, by reducing the expression of ADCY1, the team eliminated many autism-like behaviors. Second, the protein’s increased expression caused increased signaling in neurons. By reducing levels of ADCY1, the team dampened neuron signaling to levels within a normal range.
Researchers have observed that a protein called SHANK prevents the spread of breast cancer cells to the surrounding tissue. The SHANK protein has been previously studied only in the central nervous system, and it is known that its absence or gene mutations are related to autism.