Monthly Archives: juni 2015

A digital map of the ageing brain could aid the diagnosis of Alzheimer’s disease and other neurodegenerative disorders in older people, a study suggests.

The atlas created using images from MRI scans of older people could aid diagnosis by comparing the patients’ scans with a detailed map of the healthy ageing brain.

Most existing MRI atlases are based on the brains of young and middle-aged people, which don’t reflect the normal changes that take place in the brain as we age, the team says. Researchers at the University of Edinburgh constructed a detailed atlas of the human brain using MRI scans from more than 130 healthy people aged 60 or over.

The team used their atlas to study brain scans taken of normal older subjects and those who had been diagnosed with Alzheimer’s disease. The atlas was able to pinpoint changes in patients’ brain structure that can be an underlying sign of the condition, researchers say.

The study is published in the journal PLOS ONE.

Dr David Alexander Dickie, of The University of Edinburgh’s Brain Research Imaging Centre and SINAPSE, who was first author of the study, said: ”We’re absolutely delighted with these preliminary results and that our brain MRI atlases may be used to support earlier diagnoses of diseases such as Alzheimer’s. Earlier diagnoses are currently our strongest defence against these devastating diseases and, while our work is preliminary and ongoing, digital brain atlases are likely to be at the core of this defence.”

Source: University of Edinburgh

’Seeding’ property provides new focus for treatment to delay progression of disorder

By identifying in spinal fluid how the characteristic mutant proteins of Huntington’s disease spread from cell to cell, researchers have created a new method to quickly and accurately track the presence and proliferation of these neuron-damaging compounds — a discovery that may accelerate the development of new drugs to treat this incurable disease.

The researchers added that the cell-to-cell ”seeding” property of these mutant proteins seems to be a critical part of the disease’s progression. Their findings also advance a new drug-discovery approach: stopping the cellular transfer of the seeding compounds. Study results appear online in the journal “Molecular Psychiatry”.

Analysis of health insurance data suggests preventive effect

Type 2 diabetes most commonly occurs in late adulthood, and it has long been known that it can affect the patient’s mental health: Patients have a greater risk of developing dementia than non-diabetics. However, how does antidiabetic medication influence this risk? Researchers have investigated this issue in a new study based on data from the years 2004 to 2010 provided by the German public health insurance company AOK. These data set comprises information about diseases and medication related to more than 145,000 men and women aged 60 and over.

The analysis confirmed previous findings that diabetics have an increased risk of developing dementia. However, it was also found that this risk can significantly be modified by pioglitazone. This drug is taken as tablets. It is applied in short-term as well as in long-term treatment of diabetes as long as the body is still capable of producing its own insulin.

”Treatment with pioglitazone showed a remarkable side benefit. It was able to significantly decrease the risk of dementia,” says co-author Gabriele Doblhammer. ”The longer the treatment, the lower the risk.” Risk reduction was most noticeable when the drug was administered for at least two years. Diabetics given this treatment developed dementia less often than non-diabetics. ”The risk of developing dementia was around 47 percent lower than in non-diabetics, i.e. only about half as large.”, she said.

Protection against nerve cell damage

Pioglitazone improves the effect of the body’s own insulin. Moreover, laboratory tests have long indicated that it also protects the nerve cells. The current results are therefore no surprise to neuroscientist Michael Heneka. ”Pioglitazone is an anti-inflammatory drug that also inhibits the deposition of harmful proteins in the brain,” he says.

However, Heneka emphasizes that the exact mechanisms are not yet understood: ”Our study suggests that pioglitazone has a preventive effect. This happens when the drug is taken before symptoms of dementia manifest. Thus, it protects in particular against Alzheimer’s, the most common form of dementia. The causes for this, whether pioglitazone only has this protective effect in diabetics or if it would also work in non-diabetics – all these questions have yet to be answered. The next logical step would therefore be clinical studies. These studies would specifically investigate the effect of pioglitazone and other antidiabetics on dementia.

Source: Eurekalert

Scientists have identified a single blood protein that may indicate the development of Mild Cognitive Impairment (MCI) years before symptoms appear, a disorder that has been associated with an increased risk of Alzheimer’s disease or other dementias.

The research, published in the journal “Translational Psychiatry”, used data from over 100 sets of twins from TwinsUK, the biggest adult twin cohort in the UK. The use of 55 identical twin-pairs in the study allowed researchers to show that the association between the blood protein and a ten year decline in cognitive ability was independent of age and genetics, both of which are already known to affect the risk of developing Alzheimer’s disease, the most common form of dementia.

The study, the largest of its kind to date, measured over 1,000 proteins in the blood of over 200 healthy individuals using a laboratory test called SOMAscan*, a protein biomarker discovery tool that simultaneously measures a wide range of different proteins. Using a computerised test, the researchers then assessed each individual’s cognitive ability, and compared the results with the measured levels of each different protein in the blood.

For the first time, they found that the blood level of a protein called MAPKAPK5 was, on average, lower in individuals whose cognitive ability declined over a ten year period.

Source: Medical Research Council, UK

An international team of researchers has developed a method for fabricating nano-scale electronic scaffolds that can be injected via syringe. Once connected to electronic devices, the scaffolds can be used to monitor neural activity, stimulate tissues and even promote regenerations of neurons.

The study entitled “Syringe-injectable electronics” was recently published in the journal Nature.

Nanotechnology and revealed an innovative method to employ tiny electronic devices in the brain, or other parts of the body, as a potential therapy for a wide range of disorders, including neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). The study was performed by researchers at the Harvard University in Cambridge, Massachusetts and the National Center for Nanoscience and Technology in China.

The team had previously shown that cardiac or nerve cells grown with embedded nano-scale electronic scaffolds could generate a so-called “cyborg” tissue. The electronic devices could then record the electrical signals generated by the tissues, and measure signal changes when cardio- or neuro-stimulating drugs were administered to the cells.

Minimally invasive targeted delivery of electronics into artificial or natural structures is however a challenge. “We were able to demonstrate that we could make this scaffold and culture cells within it, but we didn’t really have an idea how to insert that into pre-existing tissue,” explained the study’s senior author Dr. Charles Lieber in a news release. Now, Dr. Lieber and colleagues have developed a pioneering method where sub-micrometer-thick mesh electronics can be delivered to their target through injection via a syringe.

Though not the first attempts at implanting electronics into the brain — deep brain stimulation has been used to treat a variety of disorders for decades — the nano-fabricated scaffolds operate on a completely different scale.

”Existing techniques are crude relative to the way the brain is wired,” Lieber explained. ”Whether it’s a silicon probe or flexible polymers…they cause inflammation in the tissue that requires periodically changing the position or the stimulation. But with our injectable electronics, it’s as if it’s not there at all. They are one million times more flexible than any state-of-the-art flexible electronics and have subcellular feature sizes. They’re what I call ”neuro-philic” — they actually like to interact with neurons.

Source: Science Daily