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Learn more quickly by transcranial magnetic brain stimulation

Learn more quickly by transcranial magnetic brain stimulation
Researchers in Bochum examine the effect of TMS

Top: Brain slice preparation through the frontal cortex of a rat showing nerve cells containing Parvalbumin (colored red) and surrounded by a perineural network (colored green) in untreated animals.
Bottom: After treating the animals with the iTBS protocol, the Parvalbumin has disappeared to a great extent. The perineural network labeled by green dye that the cells still exist, but have not been destroyed by the stimulation.

From the January 28, 2011 Eureka news alert

What sounds like science fiction is actually possible: thanks to magnetic stimulation, the activity of certain brain nerve cells can be deliberately influenced. What happens in the brain in this context has been unclear up to now. Medical experts from Bochum under the leadership of Prof. Dr. Klaus Funke (Department of Neurophysiology) have now shown that various stimulus patterns changed the activity of distinct neuronal cell types. In addition, certain stimulus patterns led to rats learning more easily. The knowledge obtained could contribute to cerebral stimulation being used more purposefully in future to treat functional disorders of the brain. The researchers have published their studies in the Journal of Neuroscience ***and in the European Journal of Neuroscience.***

Magnetic pulses stimulate the brain

Transcranial magnetic stimulation (TMS) is a relatively new method of pain-free stimulation of cerebral nerve cells. The method, which was presented by Anthony Barker for the first time in 1985, is based on the fact that the cortex, the rind of the brain located directly underneath the skull bone, can be stimulated by means of a magnetic field. TMS is applied in diagnostics, in fundamental research and also as a potential therapeutic instrument. Used in diagnostics, one single magnetic pulse serves to test the activability of nerve cells in an area of the cortex, in order to assess changes in diseases or after consumption of medications or also following a prior artificial stimulation of the brain. One single magnetic pulse can also serve to test the involvement of a certain area of the cortex in a sensorial, motoric or cognitive task, as it disturbs its natural activity for a short period, i.e. “switches off” the area on a temporary basis.

Repeated stimuli change cerebral activity

Since the mid-1990’s, repetitive TMS has been used to make purposeful changes to the activability of nerve cells in the human cortex: “In general, the activity of the cells drops as a result of a low-frequency stimulation, i.e. with one magnetic pulse per second. At higher frequencies from five to 50 pulses per second, the activity of the cells increases”, explained Prof. Funke. Above all, the researchers are specifically addressing with the effects of specific stimulus patterns like the so-called theta burst stimulation (TBS), in which 50 Hz bursts are repeated with 5 Hz. “This rhythm is based on the natural theta rhythm of four to seven Hertz which can be observed in an EEG“, says Funke. The effect is above all dependent on whether such stimulus patterns are provided continuously (cTBS, attenuating effect) or with interruptions (intermittent, iTBS, strengthening effect).

Contact points between cells are strengthened or weakened

It is unknown to a great extent how precisely the activity of nerve cells is changed by repeated stimulation. It is assumed that the contact points (synapses) between the cells are strengthened (synaptic potentation) or weakened (synaptic depression) as a result of the repeated stimulation, a process which also plays an important role in learning. Some time ago, it was also shown that the effects of TMS and learning interact in humans.

Inhibitory cortical cells react particularly sensitive to stimulation

The researchers in Bochum have now shown for the first time that an artificial cortex stimulation specifically changes the activity of certain inhibitory nerve cells as a function of the stimulus protocol used. The balanced interaction of excitatory and inhibitory nerve cells is the absolute prerequisite for healthy functioning of the brain. Nerve cells specialised in inhibition of other nerve cells show a much greater variety in terms of cell shape and activity structure than their excitatory counterparts. Amongst other things, they produce various functional proteins in their cell body. In his studies, Prof. Funke has concentrated on the examination of the proteins Parvalbumin (PV), Calbindin-D28k (CB) and Calretinin (CR). They are formed by various inhibitory cells as a function of activity, with the result that their quantity gives information about the activity of the nerve cells in question.

Stimulus patterns act specifically on certain cells

For example, the examinations showed that activating stimulation protocol (iTBS) almost only reduces the PV content of the cells, whereas continuous stimulation attenuating activity (cTBS protocol), or a likewise attenuating 1 Hz stimulation, mainly reduces the CB production. CR formation was not changed by any of the tested stimulus protocols. Registration of the electrical activity of nerve cells confirmed a change in inhibition of the cortical activity.

Learning more quickly after stimulation

In a second study, recently published in the European Journal of Neuroscience, Prof. Funke’s group was able to show that rats also learned more quickly if they were treated with the activating stimulus protocol (iTBS) before each training, but not if the inhibiting cTBS protocol has been used. It was seen that the initially reduced formation of the protein Parvalbumin (PV) was increased again by the learning procedure, but only in the areas of the brain involved in the learning process. For animals not involved in the specific learning task, production of PV remained reduced following iTBS. “The iTBS treatment therefore initially reduces the activity of certain inhibiting nerve cells more generally, with the result that the following learning activities can be stored more easily,” concludes Prof. Funke. “This process is termed “gating”. In a second step, the learning activity restores the normal inhibition and PV production.”

More purposeful treatment in future

Repetitive TMS is already being used in clinical trials with limited success for therapy of functional disorders of the brain, above all in severe depressions. In addition, it was shown that especially disorders of the inhibitory nerve cells play an important role in neuropsychiatric diseases such as schizophrenia. “It is doubtless too early to derive new forms of treatment of functional disorders of the brain from the results of our study, but the knowledge obtained provides an important contribution for a possibly more specific application of TMS in future”, is Prof. Funke’s hope.

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Related article

Learning causes structural changes in affected neurons
When a laboratory rat learns how to reach for and grab a food pellet — a pretty complex and unnatural act for a rodent — the acquired knowledge significantly alters the structure of the specific brain cells involved, which sprout a whopping 22 percent more dendritic spines connecting them to other motor neurons.

January 31, 2011 Posted by | Medical and Health Research News | , , , , , , | Leave a comment

Researchers discover age of onset of puberty predicts adult osteoporosis risk

Researchers discover age of onset of puberty predicts adult osteoporosis risk
Later puberty results in lower bone mass and increases risk of fracture

Vicente Gilsanz, M.D., Ph.D., is director of clinical imaging at the Saban Research Institute of Children’s Hospital Los Angeles.

From the January 28, 2011 Eureka news alert

LOS ANGELES (January 27, 2011) – A team of researchers led by Vicente Gilsanz, MD, PhD, director of Clinical Imaging at The Saban Research Institute of Children’s Hospital Los Angeles, determined that the onset of puberty was the primary influence on adult bone mineral density, or bone strength. Length of puberty did not affect bone density.

Reduced bone mineral density leads to osteoporosis, resulting in bones becoming increasingly brittle and at risk for fracture. Osteoporosis is a significant public health issue with the cost of treatment in 2010 estimated at $10 billion. This condition affects 55% of Americans aged 50 and older.

The Bone Mineral Density in Childhood Study is an ongoing multicenter study examining bone development in healthy children and teenagers of both sexes and ethnic groups in the United States. For this analysis, the investigators studied 78 girls and 84 boys who had just entered puberty, until they reached sexual maturity.

“Puberty has a significant role in bone development,” explained Dr. Gilsanz. “During this time, bones lengthen and increase in density. At the end of puberty the epiphyseal plates close, terminating the ability of the bones to lengthen. When this occurs, the teenager has reached their maximum adult height and peak bone mass. We found that early puberty was associated with greater bone mass while later puberty resulted in less.”

Adolescents with short stature sometimes undergo medical intervention to delay puberty in an effort to achieve greater height. This study indicates that prolonging the growth period by delaying puberty may have unexpected consequences in later life.

The 2000 National Institutes of Health Consensus Development Conference on Osteoporosis Prevention, Diagnosis, and Therapy identified bone mineral deposition during adolescence as a critical determinant of osteoporosis risk later in life. The care of patients with osteoporosis is difficult, and most therapies increase bone density by small amounts yet requires long periods of treatment. In contrast, during puberty large increases in bone density occur over a short period of time.

Given that the rate of decline of bone mass in adulthood is approximately 1% to 2% each year, a 10% to 20% increase in bone density resulting from a natural early puberty corresponds to an additional 10 to 20 years of protection against the normal age-related decline in bone strength.

 

January 31, 2011 Posted by | Consumer Health, Medical and Health Research News | , , , | Leave a comment

Cold cases gone hot: Montreal researchers solve decades-old medical mysteries using genetics

Cold cases gone hot: Montreal researchers solve decades-old medical mysteries using genetics
Studies published in the New England Journal of Medicine and JAMA within a week of each other

From the January 28, 2009 Eureka news alert

Montreal, January 28, 2011 – The mystery began in 1976. Adolfo Pampena was diagnosed with a rare form of cancer that caused a strange combination of symptoms and was associated with the occurrence of multiple tumours in his stomach and colon. His medical team was stumped and was unable to answer the most important questions for him and his family: the cause of his disease and the risk for future generations.

Now, 35 years later, the answers are at hand thanks to a genetic study led by investigators at the Research Institute of the McGill University Health Centre (RI MUHC), the McGill Program in Cancer Genetics at the Gerald Bronfman Centre for Clinical Research in Oncology and the Lady Davis Institute for Medical Research at the Jewish General Hospital. The study was recently published in The New England Journal of Medicine.***

The researchers were able to pinpoint the gene responsible for the disease (BUB1B), which is involved in the regulation of chromosomal separation. Instability during cell division can result in chromosomes ending up in the wrong place, which can lead to the development of tumours. “The general significance of this discovery is that individuals can be seen at our genetic clinic with an unknown condition and end up with a diagnosis that is relevant to patients and their families,” said Dr. William Foulkes, senior author of the study and a researcher in genetics at the RI MUHC, the Lady Davis Institute.

“My father and family were relieved that the cancer risk for other family members is much less than we thought,” said Mary Pampena, Adolfo’s daughter. “Now we know more about my father’s genetic history and the cancers he had. We know what screening test to do in the future. This is important information for us, our children and future generations.”

In another study published in the January, 2011 Journal of the American Medical Association (JAMA)***. Dr. Foulkes details a second solved mystery involving five families with a long history of nontoxic multinodular goiter (MNG). Goiter is a thyroid disease which can lead to extreme swelling of the neck or larynx. The most common form of the disease is not genetic and is due to iodine insufficiency. However, this form of MNG was known to be genetic, but to date, no one had ever localized the specific gene or mutation responsible. Dr. Foulkes, Dr. Marc Tischkowitz (from the Program in Cancer Genetics and the Lady Davis Institute) and their team finally succeeded, and found the mutation in a surprising place.

As it turns out, the mutation, in a gene called DICER1, was extremely unusual, Foulkes said, who is also James McGill Professor of Medicine, Human Genetics and Oncology and Director of the Program in Cancer Genetics at McGill University. “It changes the protein in only one place, and that single change is enough to trigger multinodular goiter. Generally speaking, when you have a mutation in a disease gene, it causes a multitude of problems, not just one illness. But in this case, we have no evidence that it causes anything except goiter.

Intriguingly, women in three of the families had been diagnosed with an unusual type of ovarian tumor called Sertoli-Leydig Cell Tumor and thus Foulkes and his colleagues were able confirm that there is a genetic link between multi-nodular goiter and these rare tumors. This link had first been postulated in 1974.

“In the future, our challenge as researchers is to be able to help people with an unknown condition by finding out rather quickly what the genetic cause of their problem is” explained Foulkes. “We can hope in the long-term to have an impact on treatment, diagnosis and other aspect of management.”

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January 31, 2011 Posted by | Medical and Health Research News | Leave a comment

   

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