Posts tagged brain
Articles and news from the latest research reports.
Dark matter DNA active in brain during day — night cycle
NIH study of rats shows DNA regions thought inactive highly involved in body’s clock
Long stretches of DNA once considered inert dark matter appear to be uniquely active in a part of the brain known to control the body’s 24-hour cycle, according to researchers at the National Institutes of Health.
Working with material from rat brains, the researchers found some expanses of DNA contained the information that generate biologically active molecules. The levels of these molecules rose and fell, in synchrony with 24-hour cycles of light and darkness. Activity of some of the molecules peaked at night and diminished during the day, while the remainder peaked during the day and diminished during the night.
How does electrical stimulation affect the brain? A project by Aalto University and the University of Helsinki, launched in early 2012, studies the impact mechanism of deep brain stimulation and develops electrochemical sensors for more effective measuring of neurotransmitters in the brain. The long-term goals of the research are more specific treatment for Parkinson’s disease and many other diseases of the nervous system.
Giving lithium to those who need it
Lithium is a ‘gold standard’ drug for treating bipolar disorder, however not everyone responds in the same way. New research published in BioMed Central’s open access journal Biology of Mood & Anxiety Disorders finds that this is true at the levels of gene activation, especially in the activation or repression of genes which alter the level the apoptosis (programmed cell death). Most notably BCL2, known to be important for the therapeutic effects of lithium, did not increase in non-responders. This can be tested in the blood of patients within four weeks of treatment.
A research team from Yale University School of Medicine measured the changing levels of gene activity in the blood of twenty depressed adult subjects with bipolar disorder before treatment, and then fortnightly once treatment with lithium carbonate had begun.
Over the eight weeks of treatment there were definite differences in the levels of gene expression between those who responded to lithium (measured using the Hamilton Depression Rating Scale) and those who failed to respond. Dr Robert Beech who led this study explained, “We found 127 genes that had different patterns of activity (turned up or down) and the most affected cellular signalling pathway was that controlled programmed cell death (apoptosis).”
For people who responded to lithium the genes which protect against apoptosis, including Bcl2 and IRS2, were up regulated, while those which promote apoptosis were down regulated, including BAD and BAK1.
The protein coded by BAK1 can open an anion channel in mitochondrial walls which leads to leakage of mitochondrial contents and activation of cell death pathways. Damage similar to this has been seen within the prefrontal cortex of the brain of patients with bipolar disorder. BAD protein is thought to promote BAK1 activity, while Bcl2 binds to BAK1 and prevents its ability to bind to the channel.
Dr Beech continued, “This positive swing in regulation of apoptosis for lithium responders was measurable as early as four weeks after the start of treatment, while in non-responders there was a measureable shift in the opposite direction. It seems then, that increased expression of BCL2 and related genes is necessary for the therapeutic effects of lithium. Understanding these differences in genes expression may lead towards personalized treatment for bipolar disorder in the future.”
(Source: biomedcentral.com)
Kangaroo Mother Care - a technique in which a breastfed premature infant remains in skin-to-skin contact with the parent’s chest rather than being placed in an incubator - has lasting positive impact on brain development, revealed Universite Laval researchers in the October issue of Acta Paediatrica. Very premature infants who benefited from this technique had better brain functioning in adolescence - comparable to that of adolescents born at term - than did premature infants placed in incubators.
A University of Arizona professor is overseeing the manufacture of an experimental drug that could help reduce brain damage after a stroke.
The drug, known as 3K3A-APC, currently is undergoing clinical trials in Europe to determine its safety in humans after proving effective in animal models at reducing brain damage and improving motor skills after a stroke when given in combination with another commonly used stroke therapy.
Thomas Davis, professor of pharmacology in the UA College of Medicine, was chosen to direct the manufacture of the drug for human trials after co-authoring a recent paper in the journal Stroke that pointed to the drug’s effectiveness in rats and mice when used in conjunction with a clot-busting therapy known as tissue plasminogen activator, or tPA.
While tPA is commonly given to sufferers of ischemic stroke, which results from an obstruction in a blood vessel supplying blood to the brain, the therapy poses significant challenges when administered alone, including a limited treatment window, Davis said.
"It has to be given within the first three to four and a half hours of the stroke," Davis said. "It only works in 10 percent of the patients, and it causes bleeding, so tPA alone isn’t that effective."
Neurodegenerative diseases such as Alzheimer’s or Parkinson’s are characterised by the loss of nerve cells and the deposition of proteins in the brain tissue. A group of researchers led by Gabor G. Kovacs from the Clinical Institute of Neurology at the MedUni Vienna has now demonstrated that Alzheimer’s disease does not just – as previously believed – involve the proteins that are attributed to Alzheimer’s, but instead the condition can involve a mixture of interacting proteins from different neurodegenerative diseases.
“As a result, Alzheimer’s should not be treated in isolation. According to these latest findings, pure, classical Alzheimer’s disease, which involves only the attributed proteins tau and amyloid beta, appears not to be the norm,” says Kovacs. There is also a varied regional distribution of nerve cell loss and protein deposits between patients which, taken together, have clinical prognostic significance. As a consequence of this, differentiated strategies need to be developed for personalised therapy that takes account of all the interacting factors.
The new treatment concepts which are currently being developed by the MedUni Vienna’s neuropathologists, neurobiologists, neurologists, psychiatrists and neuroimaging experts will divide the patients into “sub-groups”. Says Kovacs: “The aim is to define these groups very precisely in future in order to be able to offer them personalised treatment.”
Dementia diseases: a growing trend
Around 100,000 Austrians are currently suffering from a dementia-related illness, according to statistics from the Austrian Alzheimer Society. According to estimates, this figure will rise to around 280,000 by 2050 as a result of the increasing age of the general population. Alzheimer’s disease is responsible for 60 to 80 per cent of these conditions.The global Alzheimer’s report by “Alzheimer’s Disease International” reckons that the prevalence of dementia doubles every 20 years. There are currently around 35 million people worldwide suffering a dementia-related illness. By 2030, their number will rise to 65.7 million and reach as many as 115.4 million by 2050.
UK scientists have made a breakthrough in a new method of brain tumor diagnosis, offering hope to tens of thousands of people.
Researchers, led by Professor Francis Martin of Lancaster Environment Centre at Lancaster University, have shown that infrared and Raman spectroscopy – coupled with statistical analysis – can be used to tell the difference between normal brain tissue and the different tumor types that may arise in this tissue, based on its individual biochemical-cell ‘fingerprint’.
Spectroscopy is a technique that allows us to analyse light interactions with samples such as tissue by generating a spectrum, which is a reflection of the interrogated sample.
Currently, when surgeons are operating to remove a brain tumor it can be difficult to spot where the tumor ends and normal tissue begins.
But new research published online in Analytical Methods this month has shown it is possible to spot the difference between diseased and normal tissue using Raman spectroscopy – a type of spectroscopy which works effectively on living tissue, giving accurate results in seconds.
At this year’s Tokyo Games Show, Japanese purveyor of electronically-augmented fashion Neurowear unveiled the successor to its Necomimi brain-activated cat ears. It’s called Shippo, and it’s a brain-controlled motorized tail that responds to the user’s current emotional state with corresponding wagging.
Shippo requires a NeuroSky electroencephalograph (EEG) headset, alongside a clip-on heart monitor, in order to observe brain activity and pick up on the user’s emotional state. This information is then translated to wagging, which will be soft and slow or hard and fast, depending on whether one is relaxing or excited/anxious. The EEG headset communicates with the fluffy appendage via a Bluetooth connection.
Vision cells, not brain, to blame for colour blindness
The real culprits of colour blindness are vision cells rather than unusual wiring in the eye and brain, recent research has shown.
The discovery brings scientists a step closer to restoring full colour vision for people who are colour blind – a condition that affects close to two million Australians, says Professor Paul Martin from The Vision Centre and The University of Sydney.
It may also help pave the way for an answer to one of the most common causes of blindness – age-related macular degeneration (AMD), which accounts for half of the legal blindness cases in Australia.
“There are millions of cones in our eyes – vision cells that pick up bright light and allow us to see colour,” Prof. Martin says. “They are nicknamed red, green and blue cones because they are sensitive to different wavelengths of light.
“We now know that in the macular region of the eye, each cone has its own ’private line’ into the optic nerve and the brain. Just as a painter can mix from three tubes of paint to produce a wide and vivid palette, our brain uses the ‘private lines’ from the three cone types to create thousands of colour sensations.
Scientists previously thought that full colour vision depends on specialised nerve wiring in the eye and brain, but animal studies show that the wiring is identical for monkeys whether they have normal or abnormal colour vision, Prof. Martin says.
“This tells us that there’s nothing wrong in the brain – it’s only working with the signals that it receives on the ‘private lines’,” he says. “So the only difference in normal and abnormal colour vision is caused by the first stage of sight, which points to faulty cones. Either they have failed to develop, or else they are picking up abnormal wavelengths.
“Now that we know faulty wiring isn’t the cause, we can concentrate on fixing the cones, which are controlled by genes – and thus prone to mutation or mistakes during cell replication. There are already promising results from gene therapy as a way to restore full colour vision in colour blind monkeys.”
“While we have still have some way to go, the benefits of this gene therapy – if successful – can potentially extend beyond providing complete colour vision,” he says.
“If we can get these genes to work in human eyes, it means that the same approach might be possible for other visual problems – including blinding diseases such as macular degeneration.”
"In macular degeneration, energy supplies to the macula can’t keep up with demand. So the ‘private line’ system must be very energy-intensive. Gene therapy could be used to turn down the cones’ energy demand, or to increase energy supply from supporting cells to cone cells,” Prof. Martin says.
“Together with clinical researchers at the Save Sight Institute, we are now working hard to find out exactly how many ‘private lines’ there are in humans. That can point us to where energy demand is highest and we can target gene therapy to the right place.
"So animal research on ‘private lines’ for colour vision has given new clues for understanding one of the most important visual diseases – macular degeneration – in humans."
(Source: scinews.com.au)
Researchers at Cold Spring Harbor Laboratory (CSHL) have solved an important piece of one of neuroscience’s outstanding puzzles: how progenitor cells in the developing mammalian brain reproduce themselves while also giving birth to neurons that will populate the emerging cerebral cortex, the seat of cognition and executive function in the mature brain.
CSHL Professor Linda Van Aelst, Ph.D., and colleagues set out to solve a particular mystery concerning radial glial cells, or RGCs, which are progenitors of pyramidal neurons, the most common type of excitatory nerve cell in the mature mammalian cortex.
In genetically manipulated mice, Van Aelst’s team demonstrated that a protein called DOCK7 plays a central regulatory role in the process that determines how and when an RGC “decides” either to proliferate, i.e., make more progenitor cells like itself, or give rise to cells that will mature, or “differentiate,” into pyramidal neurons. The findings are reported in the September 2012 issue of Nature Neuroscience