Down's syndrome girl attacked and beaten by girl gang in UK park

A 12-year-old with Down's syndrome has been hospitalised by a vicious girl gang who beat her up in a park.

The youngster was playing in a local park in Bobby Heywood Park, Great Lever, Bolton, Manchester, when she was assaulted by a group of older girls.

The girl was taken to Manchester Children's Hospital with a serious head injury. At first the girl said she had fallen off a swing, after the incident on Wednesday but her family later reported to police on Friday that she had been attacked.

Police are now appealing for anyone who may have been in the park at the time, or has any information about what happened, to contact them.

Detectives are yet to interview the girl as she is still “unwell in hospital”, police said.

Insp Andy Sidebotham, said: "This incident has quite rightly caused a lot of concern both in the community and on social media networks and I want to reassure everyone that we are taking this extremely seriously.

"Due to the girl's obvious vulnerability, this case is clearly very emotive, but I want to stress to everyone that we have launched a painstaking investigation to get to the bottom of what happened.

"It is important that officers are allowed to do our jobs and get on with catching those responsible.

"With that in mind we have been speaking to the victim, her family and witnesses, but we still want to hear from anyone who may have been in the playground last Wednesday afternoon.

The Manchester police are asking the public to come forward with any information they may have.

Down's syndrome: Further insight into complex Neuropathology

Researchers at the University of Bristol have revealed new insight into the function of a key protein attributed to impaired learning and memory in Down's syndrome.

The findings, published online in Nature Cell Biology, offer further molecular insight into how the reduced level of this key protein termed 'sorting nexin-27' [SNX27] may contribute to learning and memory problems associated with Down's syndrome.

The Bristol-based team now reveal how SNX27 forms the core component of an ancient protein complex which functions to control the abundance of a select group of proteins at the surface of cells.

Included among these proteins are numerous transporters that regulate the cell's ability to take up various nutrients, including glucose and metal ions such as zinc and copper.

In cells lacking SNX27, the level of these transporters is reduced and the cell's ability to take up nutrients is adversely perturbed.

Peter Cullen

Peter Cullen, Professor of Biochemistry from the University's School of Biochemistry and senior author of the Wellcome Trust-funded study, said: "Besides the previously recognised role of SNX27 in regulating the synaptic activity of neurones, our study suggests that the lack of SNX27 expression observed in Down's syndrome may also lead to a reduced metabolic activity that may adversely affect neuronal development and cognitive function.

"Further analysis of the effect of reduced SNX27 expression on the synaptic and metabolic activity of specific neuronal populations will certainly provide much needed molecular insight into the complex neuropathology of Down's syndrome as well as other neurological conditions."

More information:
Steinberg F. et al. A global analysis of SNX27-retromer assembly and cargo specificity reveals a function in glucose and metal ion transport, Nature Cell Biology.

Down's syndrome 'linked to brain protein loss'

A lack of a protein in Down's syndrome brains could be the cause of learning and memory problems, says a US study.

Writing in Nature Medicine, Californian researchers found that the extra copy of chromosome 21 in people with the condition triggered the protein loss.

Their study found restoring the protein in Down's syndrome mice improved cognitive function and behaviour.

The Down's Syndrome Association said the study was interesting but the causes of Down's were very complex.

Prof Huaxi Xu, senior author of the study from the Sanford-Burnham Medical Research Institute, said that in experiments on mice they discovered that the SNX27 protein was important for brain function and memory formation.

Mice with less SNX27 had fewer active glutamate receptors and therefore had impaired learning and memory.

The SNX27-deficient mice shared some characteristics with Down's syndrome, so the researchers looked at human brains with the condition.

This confirmed their findings in the lab - that people with Down's syndrome also have significantly lower levels of SNX27.

Neurons from a normal mouse (left) are longer and fuller than neurons from a mouse lacking SNX27 (right)

"So, in Down's syndrome, we believe lack of SNX27 is at least partly to blame for developmental and cognitive defects," Prof Xu said.

In the lab, the research team increased the levels of the protein in mice brains to see if the problem could be resolved.

"Everything goes back to normal after SNX27 treatment," said Xin Wang, a graduate member of the research team.

"First we see the glutamate receptors come back, then memory deficit is repaired in our Down's syndrome mice."

But Prof Xu cautioned that science still had work to do to develop a safe technique of delivering genes into the human brain.