Acupuncture stimulates brain metabolism in dementia patients

CM NEWS – Needling specific acupoints may help patients with dementia, a recently published study shows. The acupoint combo seems to increase cerebral glucose metabolism in the brain, as indicated by cerebral functional imaging.

The study has been published in the January 2007 issue of the Journal of Acupuncture and Tuina Science. Chinese researchers observed the effects of needling three acupoints – Baihui (百會, Hundred Convergences; GV 20), Shuigou (水溝, Water Trough; GV 26) and Shenmen (神門, Spirit Gate; HT 7) – and their effects on cerebral glucose metabolism in patients with vascular dementia.

25 patients with vascular dementia were divided into 5 groups (Group A, B, C, D and E) randomly. Patients in the Group A were treated by needling routine acupoints for hemiplegia (paralysis in the vertical half of a patient’s body), which are acupoints of the three “yang meridians” of the hand and foot.

In addition to the “routine acupoints”, Group B patients received acupuncture to Baihui (GV 20); Group C to Shuigou (GV 26), Group D to Shenmen (HT 7), and Group E to Baihui (GV 20), Shuigou (GV 26), and Shenmen (HT 7).

All the patients were examined by Positron Emission Tomography (PET) to detect cerebral glucose metabolism in the bilateral frontal lobes (orbital gyri), parietal lobes, temporal lobes (hippocampus and hippocampal gyrus), occipital lobes, thalamus, lentiform nucleus, caudate nuclei, cingulate gyms and cerebellum before treatments and after treatments.

Why checking on cerebral glucose metabolism? Studies have linked dementia with the slowing of glucose metabolism in certain parts of the brain. One study indicated that patients with frontotemporal dementia not only showed significant metabolic deficits primarily in frontal cortical areas, but also in the caudate nuclei and the thalami. These findings demonstrate that the clinical progression in patients with frontotemporal dementia is accompanied by a region-specific decline in cerebral glucose metabolism.

Another study found that patients with multi-infarct dementia (MID) had significantly lower glucose metabolism in all the grey matter regions measured and were also characterized by more individuality in metabolic pattern.

The present study shows that after needling the routine acupoints for hemiplegia, glucose metabolism increased in lentiform nucleus and temporal lobe; and:

* patients with Baihui (GV 20) needled showed increased glucose metabolism in the frontal lobe, temporal lobe and lentiform nucleus.
* patients with Shuigou (GV 26) needled showed increased glucose metabolism in the frontal lobe, thalamus and lentiform nucleus;
* patients with Shenmen (HT 7) needled got more glucose metabolism in the parietal lobe and lentiform nucleus;
* patients who recieved needling to all these three acupoints has higher glucose metabolism in the frontal lobe, temporal lobe, thalamus and lentiform nucleus.

The results suggest that needling Baihui (GV 20), Shuigou (GV 26) and Shenmen (HT 7) affect glucose metabolism in different functional regions of the brain. In other words, the three acupoints are closely correlated to different functional regions of the brain.

Vitamin D helps brain to work well at later age

Vitamin D may have a key role in helping the brain to keep working well in later life, suggests research published ahead of print in the Journal of Neurology Neurosurgery and Psychiatry.

Previous research indicates that inadequate vitamin D intake may be linked to poorer mental agility in the ageing brain, but the results have been inconsistent.
The researchers base their current findings on just over 3000 European men between the ages of 40 and 79, who were all part of the international European Male Ageing Study, drawn from eight different cities across Europe.

Their mental agility was assessed using a range of tests, designed to measure memory and speed of information processing as well as mood and physical activity levels, both of which affect mental agility.

Blood samples were then taken to measure circulating levels of vitamin D, which is obtained through dietary sources and by exposure to sunlight.

High circulating vitamin D levels were associated with high scores on the memory and information processing tests, but after adjusting for mood and physical activity, the association remained for only one of the two information processing tests.

Low vitamin D levels were associated with poor scores, with levels of 35 nmol/litre or under marking the threshold of poorer performance.

Experimental data point to the biological plausibility for an association between low circulating levels of vitamin D and poorer mental agility, but exactly how the two might be connected is not clear, say the authors.

Possible suggestions include vitamin D’s role in increasing certain hormonal activity or the protection of neurones and chemical signalling pathways.

The findings show that the magnitude of the association between vitamin D level and mental agility was comparatively small, say the authors.

But if it were possible to stave off the effects of ageing on the brain with vitamin D supplements, then the implications for population health could be quite significant, they contend, because many people, particularly in older age, arevitamin D deficient.

Damaging Inflammatory Response Could Hinder Spinal Cord Repair

ScienceDaily (Oct. 22, 2009) — The inflammatory response following a spinal cord injury appears to be set up to cause extra tissue damage instead of promoting healing, new research suggests.
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Scientists analyzing this inflammatory response in mice discovered that the types of cells recruited to the site of the injury are dominated within a week by those that promote inflammation. When chronic, inflammation can prevent healing, and these inflammatory cells are believed to remain at the injury site indefinitely.

Meanwhile, similar cells that are typically involved in a later phase of injury repair and that are anti-inflammatory were found to promote effective growth of axons that connect nerve cells. However, these cells disappear shortly after an injury, making it unlikely that they get a chance to complete their work under naturally occurring circumstances.

All of the responding cells in question are macrophages, but the study revealed that they have slightly different characteristics that define their functions. The research suggests that changing the balance of how these cells are activated in favor of the anti-inflammatory macrophages could be a potential treatment strategy for spinal cord injury.

Currently, no Food and Drug Administration-approved treatment exists for spinal cord injury, and scientists have not discovered a way to repair nerve cells that are damaged or killed when the spinal cord is injured. An estimated 1.3 million people in the United States are living with a spinal cord injury, experiencing paralysis and complications that include bladder, bowel and sexual dysfunction and chronic pain.

“If these pro-inflammatory macrophages are a big part of the reason cells are dying, and we can figure out how to shut off that death cascade that they start, we might be able to minimize the amount of tissue damage,” said senior study author Phillip Popovich, a professor of neuroscience and molecular virology, immunology and medical genetics at Ohio State University.

“If that could be achieved by injecting a drug or giving a patient a pill for a set number of days after injury, that could improve a lot of function and quality of life for people who suffer a spinal cord injury.”

The research was presented Wednesday during a poster session at the Society for Neuroscience annual meeting in Chicago.

Popovich has known about the presence of macrophages after spinal cord injury for a long time. What he didn’t know was exactly what they did, or how they did it, or whether there could be more than one function among these cells.

“I’ve always been of the mind that if nature requires these cells to be there, we must figure out if it’s advantageous or disadvantageous for spinal cord function,” said Popovich, also director of Ohio State’s Center for Brain and Spinal Cord Repair.

“If what they do is disadvantageous, how can we change that without completely removing them? Because if we remove them, it will probably change a lot of other things and that is not going to be beneficial.”

In this study, he and colleagues compared the spinal cords of mice with injury to the spinal cords of uninjured mice. The mouse injuries resembled the most common contusion/compression spinal cord damage in humans that occurs when a vertebral bone or a disc bumps into the cord, causing a lesion and bleeding.

The researchers used chemicals to stain the spinal cords with markers that would indicate what types of cells were active at the injury site. They named the pro-inflammatory macrophages M1 cells and anti-inflammatory macrophages M2 cells.

Immediately after the injury, the researchers observed an intermingling of M1 and M2 cells at the site of the spinal cord injury. In just a few days, all of the anti-inflammatory M2 cells had disappeared. The pro-inflammatory M1 population persisted for a month after injury — the longest period scientists have ever observed.

Popovich said he and colleagues used recent principles learned by others in models of repair of injured heart muscle to predict how the inflammatory response to spinal cord injury would occur. After the heart is damaged, macrophages migrate to the site to clean up debris and protect against any invading bacteria or other pathogens. Signals are eventually sent out to initiate a next phase, which prepares the site for repair. Then new cells are recruited, blood vessels grow and other macrophages facilitate closure of the wound.

In the spinal cord, the long-term presence of pro-inflammatory M1 cells appears to prevent the shift into a repair phase.

“What we’ve done is overly simplistic, but it’s an advance conceptually from where we were because we’re saying that even though it looks like a homogeneous response, not all macrophages are created equal,” Popovich said.

Once they knew how M1 and M2 cells were distributed at an injury site, the researchers sought to determine what those two types of macrophages could do.

They created in vitro models — essentially, test tube experiments — in which they examined the effects of M1 and M2 macrophages on neurons, the cells that make up most of the spinal cord and brain.

The M1 macrophages killed neurons or stimulated a sprouting type of growth among their axons, which function as arms on neurons that reach out to connect with other cells or to send and receive signals. This type of sprouting of axons is associated with misguided circuits and can actually cause chronic pain.

The M2 cells, on the other hand, promoted long-distance axon growth without causing toxicity. This is the kind of axon growth required to regenerate spinal cord tissue and is the type of axon growth that is normally inhibited by proteins and cells that accumulate in the spinal cord after injury.

Popovich speculates that the immune system normally inhibits axon regeneration because its primary goal is to keep the injured spinal cord free from infection.

“The injury opens tissue to the external environment, increasing the potential to be exposed to pathogens. The immune system doesn’t care that the spinal cord is damaged — it just wants to keep the organism alive,” he said. “And neurons want to regrow, but when they try to grow their axons, they hit a wall of inflammatory cells that they can’t get past or that are working against them.”

One class of drugs — PPARgamma agonists, used to treat diabetes — is known to promote recruitment of M2 macrophages and has appeared in previous research to protect neurons in models of spinal cord injury, Popovich said. But before pursuing drug therapies, researchers must determine whether changing the balance of macrophages in an injured spinal cord to favor the activation of M2 cells would actually be beneficial in a human body.

“The only benefits we’ve shown so far were in vitro,” he said. “There’s a chance we’ll never be able to figure out how to regenerate an axon. But if we could minimize damage caused by inflammation, that would be helpful. Each axon that dies gets you closer to a threshold where you lose function. If we could just keep axons and neurons alive, we may have a better chance at promoting recovery.”

The National Institutes of Health and the National Institute of Neurological Disorders and Stroke supported this research.

Popovich conducted the work with postdoctoral researchers Kristina Kigerl and John Gensel, and research scientist Daniel Ankeny, all of Ohio State’s Department of Molecular Virology, Immunology and Medical Genetics; Jessica Alexander of the Neuroscience Graduate Studies Program; and graduate student Dustin Donnelly of the Medical Scientist Program. All of the co-authors also are also investigators in the Center for Brain and Spinal Cord Repair.

Monkey brains signal the desire to explore

DURHAM, N.C. Sticking with what you know often comes at the price of learning about more favorable alternatives.

Managing this trade-off is easy for many, but not for those with conditions such as Alzheimer’s disease or obsessive-compulsive disorder who are trapped in simple routines.

Using brain scans in monkeys, Duke University Medical Center researchers are now able to predict when monkeys will switch from exploiting a known resource to exploring their options.

“Humans aren’t the only animals who wonder if the grass is greener elsewhere, but it’s hard to abandon what we know in hopes of finding something better,” said John Pearson, Ph.D., research associate in the Duke Department of Neurobiology and lead author of a study published in this week’s Current Biology.

“Studies like this one help reveal how the brain weighs costs and benefits in making that kind of decision,” Pearson said. “We suspect that such a fundamental question engages many areas of the brain, but this is one of the first studies to show how individual neurons can carry signals for these kinds of strategic decisions.”

The researchers looked at how nerve cells fired in a part of the brain known as the posterior cingulate cortex as the monkeys were offered a selection of rewards. Generally, these neurons fired more strongly when monkeys decided to explore new alternatives.

The monkeys started with four rewards to choose from, each a 200 microliter cup of juice. After that, the four targets began to slowly change in value, becoming larger or smaller. The monkeys were free to explore the other targets or stay with the initial target, whose value they knew for certain. Monkeys had to select an option to learn its current value and integrate this information with their knowledge of the chances of getting more juice at a different target.

By studying the individual neurons, the researchers could predict which strategy the mo

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Vitamin C Deficiency Impairs Early Brain Development, Guinea Pig Study Finds

New research at LIFE – Faculty of Life Sciences at University of Copenhagen shows that vitamin C deficiency may impair the mental development of new-born babies.

In the latest issue of the well-known scientific journal The American Journal of Clinical Nutrition, a group of researchers headed by professor Jens Lykkesfeldt shows that guinea pigs subjected to moderate vitamin C deficiency have 30 per cent less hippocampal neurones and markedly worse spatial memory than guinea pigs given a normal diet. Like guinea pigs, human beings are dependent on getting vitamin C through their diet, and Jens Lykkesfeldt therefore speculate that vitamin C deficiency in pregnant and breast-feeding women may also lead to impaired development in foetuses and new-born babies.

The brain retains vitamin C

Several factors indicate that the neonatal brain, in contrast to other tissue, is particularly vulnerable to even a slight lowering of the vitamin C level. The highest concentration of vitamin C is found in the neurons of the brain and in case of a low intake of vitamin C, the remaining vitamin is retained in the brain to secure this organ. The vitamin thus seems to be quite important to brain activity. Tests have shown that mouse foetuses that were not able to transport vitamin C develop severe brain damage. Brain damage which resembles the ones found in premature babies and which are linked to learning and cognitive disabilities later in life.

Widespread vitamin C deficiency

In some areas in the world, vitamin C deficiency is very common – population studies in Brazil and Mexico have shown that 30 to 40 per cent of the pregnant women have too low levels of vitamin C, and the low level is also found in their foetuses and new-born babies. It is not yet known to what extent new-born babies in Denmark or the Western World suffer from vitamin C deficiency but a conservative estimate would be 5 to 10 per cent based on the occurrence among adults.

“We may thus be witnessing that children get learning disabilities because they have not gotten enough vitamin C in their early life. This is unbearable when it would be so easy to prevent this deficiency by giving a vitamin supplement to high-risk pregnant women and new mothers” says Jens Lykkesfeldt whose research group is currently studying how early in pregnancy vitamin C deficiency affects the embryonic development of guinea pigs and whether the damage may be reversed after birth.

Brain Cancer

What is brain cancer?

Brain cancer is a disease of the brain in which cancer cells (malignant) arise in the brain tissue. Cancer cells grow to form a mass of cancer tissue (tumor) that interferes with brain functions such as muscle control, sensation, memory, and other normal body functions. Tumors composed of cancer cells are called malignant tumors, and those composed of noncancerous cells are called benign tumors. Cancer cells that develop from brain tissue are called primary brain tumors while tumors that spread from other body sites to the brain are termed metastatic brain tumors. Statistics suggest that brain cancer occurs infrequently and is likely to develop in about 22,000 new people per year in 2009, with about 13,000 deaths as estimated by the National Cancer Institute (NCI).

Not all brain tumors are alike, even if they arise from the same type of brain tissue. Tumors are assigned a grade depending on how the cells in the tumor appear microscopically. The grade also provides insight as to the cell’s growth rate. NCI lists the following grades:

• Grade I: The tissue is benign. The cells look nearly like normal brain cells, and they grow slowly.
• Grade II: The tissue is malignant. The cells look less like normal cells than do the cells in a grade I tumor.
• Grade III: The malignant tissue has cells that look very different from normal cells. The abnormal cells are actively growing (anaplastic).
• Grade IV: The malignant tissue has cells that look most abnormal and tend to grow quickly.

The most common primary brain tumors are usually named for the brain tissue type from which they originally developed. These are gliomas, meningiomas, pituitary adenomas, vestibular schwannomas, and primitive neuroectodermal tumors (medulloblastomas). Gliomas have several subtypes which include astrocytomas, oligodendrogliomas, ependymomas, and choroid plexus papillomas. When the grades are coupled with the tumor name, it gives doctors a better understanding about the severity of the brain cancer. For example, a grade III (anaplastic) glioma is an aggressive tumor, while an acoustic neuroma is a grade I benign tumor. However, even benign tumors can cause serious problems if they grow big enough to cause increased intracranial pressure or obstruct vascular structures or cerebrospinal fluid flow.

What is metastatic brain cancer?

Cancer cells that develop in a body organ such as the lung (primary cancer tissue type) can spread via the bloodstream or lymphatic system to other body organs such as the brain. Tumors formed by such cancer cells that spread (metastasize) to other organs are called metastatic tumors. Metastatic brain cancer is a mass of cells (tumor) that originated in another body organ and has spread into the brain tissue. Metastatic tumors in the brain are more common than primary brain tumors. They are usually named after the tissue or organ where the cancer first developed (for example, metastatic lung or breast cancer tumors in the brain, which are the most common types found).

What causes brain cancer?

Primary brain tumors arise from many types of brain tissue (for example, glial cells, astrocytes, and other brain cell types). Metastatic brain cancer is caused by the spread of cancer cells from a body organ to the brain. However, the causes for the change from normal cells to cancer cells in both metastatic and primary brain tumors are not fully understood. Data gathered by research scientists show that people with certain risk factors are more likely to develop brain cancer. Individuals with risk factors such as having a job in an oil refinery, as a chemist, embalmer, or rubber-industry worker show higher rates of brain cancer. Some families have several members with brain cancer, but heredity as a cause for brain tumors has not been proven. Other risk factors such as smoking, radiation exposure, and viral infection (HIV) have been suggested but not proven to cause brain cancer. There is no good evidence that brain cancer is contagious, caused by head trauma, or caused by cell phone use. Although many lay press and Web articles claim that aspartame (artificial sweetener) causes brain cancer, as of 2009, the FDA maintains that it does not cause brain cancer and base their findings on over 100 toxicological and clinical studies regarding the sweetener’s safety.

Why don’t brain tumors respond to medication?

Malignant brain tumors often fail to respond to promising new medication. Researchers in Heidelberg have discovered a mechanism and a tumor marker for the development of this resistance. A “death receptor” can possibly provide information as to how great the chances of success are for chemotherapy. At the same time, it offers a new approach for promising brain tumor therapy.

Dr. Wolf Mller, senior consultant in the Neuropathology Department at the Institute of Pathology of Heidelberg University Hospital, and his team were able to show that certain brain tumors (astrocytomas) can deactivate a crucial protein on their cell surface, the so-called death receptor. The medication docks onto this receptor and causes the cells to die. An intact “death receptor” can thus serve as a tumor marker for whether or not a therapy has a chance of success. The study was conducted with funding from the Tumor Center of Heidelberg/Mannheim and was published in the journal Clinical Cancer Research.

Primary brain tumors that develop from brain cells, in particular their most malignant variant the glioblastoma, have a very poor prognosis. Although various kinds of therapies are attempted, patients with a glioblastoma usually die within two years of diagnosis. The researchers are thus working at high speed to become more familiar with the biology of these tumors in order to develop more efficient treatment.

“Death receptor” can be switched on and off

The researchers in Heidelberg examined various primary brain tumors (astrocytomas, which also include glioblastomas) and discovered that the gene for the death receptor DR4 was switched off in up to 75 percent of cases by what is known as “promoter methylation”. This means that methyl groups accumulate at the segment of the gene that is crucial for its activity (expression). The gene’s information can thus no longer be read, the gene is silenced.

The death receptor DR4 is an attracti
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Contact: Dr. Wolf C. Mller Wolf.Mueller@med.uni-heidelberg.de 062-215-639-912 University Hospital Heidelberg Source:Eurekalert