Karen Vieira, MBA, PhD – Brain Blogger http://brainblogger.com Health and Science Blog Covering Brain Topics Wed, 30 May 2018 15:00:03 +0000 en-US hourly 1 https://wordpress.org/?v=4.9.6 New Technology for Intracranial Aneurysms http://brainblogger.com/2008/06/19/new-technology-for-intracranial-aneurysms/ http://brainblogger.com/2008/06/19/new-technology-for-intracranial-aneurysms/#comments Thu, 19 Jun 2008 13:46:13 +0000 http://brainblogger.com/?p=816 Neuroscience and Neurology CategoryAn intracranial aneurysm can be defined as a thin sac that develops in the brain through the swelling of a weakened blood vessel. As the swelling increases, the wall of the blood vessel (aneurysm) becomes weaker and runs the risk of causing a stroke if it ruptures in the patient’s brain. Most patients who suffer from an intracranial aneurysm need vascular reconstructive surgery to prevent the aneurysm from rupturing.

Current treatments include open surgical clipping of an aneurysm, which is a highly invasive procedure that involves opening the patient’s skull. This is a risky procedure that has a 12% mortality/morbidity rate and patients are required to stay in the hospital for three or four days after the operation. A second form of treatment involves less invasive neurovascular techniques such as the occlusion of the parent blood vessel that the aneurysm developed from. However, this type of treatment runs the risk of causing distal cerebral embolism: the blockage of a blood vessel by a foreign object, a piece of somatic tissue, a blood clot, or an air bubble.

AneurysmDr. Demetrius Lopes (a neurosurgeon) and Dr. Thomas Grobelny (a neuroradiologist) from the Neurologic & Orthopedic Institute of Chicago recently performed the first minimally invasive neuroendovascular procedure with a system called the Cordis Enterprise Vascular Reconstruction Device. The patient was a 58 year old woman diagnosed with an aneurysm based on symptoms that included problems maintaining her balance and ringing in her ears.

Neuroendovascular surgery combines the use of an x-ray, catheters, and clotting agents to treat brain and spine diseases that affect blood vessels. Surgeons place catheters into damaged blood vessels and fill the vessels with clotting agents. The procedure is normally performed in a fluoroscopy room instead of an operating room.

The technique that was designed by Dr. Lopes and Dr. Grobelny involves filling the aneurysm (via a catheter) with coils to obstruct blood flow to the aneurysm. In addition to coils, stents (wire mesh) are placed in the blood vessel to maintain the position of the coils and reconstruct the weakened blood vessel. The purpose of this advanced procedure is to stop blood flow to the aneurysm and restore normal blood flow to the parent blood vessel in a minimally invasive way.

According to Dr. Lopes, this technique can be used to treat more types of aneurysms than other techniques (e.g. open clipping or artery occlusion) because it is currently the least invasive neurological procedure. In addition, this procedure obstructs the aneurysm, thereby preventing it from rupturing and bleeding into the brain. The rupturing of an aneurysm can cause a hemorrhagic stroke. Dr. Lopes also stated that in the past, even if a patient was diagnosed with an aneurysm, if they did not present any symptoms, surgery was not a recommended form of treatment because it was too risky and invasive. The Enterprise Vascular Reconstruction procedure allows neurosurgeons and neuroradiologists to use the patient’s circulatory system to place catheters into the parent blood vessel and obstruct the aneurysm without have to open the patient’s skull.

Video

There are no published journal articles about the procedure yet, but videos of successful coiling procedures can be viewed from the Neurologic & Orthopedic Hospital of Chicago.

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More Reasons To Eat Blueberries http://brainblogger.com/2008/05/21/more-reasons-to-eat-blueberries/ http://brainblogger.com/2008/05/21/more-reasons-to-eat-blueberries/#comments Wed, 21 May 2008 14:44:07 +0000 http://brainblogger.com/?p=938 Neuroscience and Neurology CategoryIt is an old adage that “we are what we eat.” Current research is proving that this is no old wives tale especially when it comes to our brains. The Peninsula Medical School and the University of Reading studied the ability of blueberries to improve memory. The results of this research showed that fruits like blueberries, which are high in phytochemicals, can improve and even reverse age-related memory deficits while offering many other health benefits for the body. The studies also show that improvements are possible for both long term and short term memory function.

To date, the mechanism of how fruits like blueberries improve memory and brain function is unclear, but it is believed that the phytochemicals they contain cross the blood brain barrier and affect learning and memory by enhancing existing neuronal (brain cell) connections. The researchers are also suggested that the improvement in memory is directly related to stimulated “signaling proteins” that can be found in the the hippocampus. The hippocampus is the part of the brain that controls memory and learning.

BlueberryAdditional research has pointed to not only the beneficial effects of blueberries, but also to the Acai berry as a powerful brain food. Acai berries are rich in antioxidants, but in addition, have high levels of essential fatty acids. Such large amounts of essential fatty acids is odd for a berry, but great since it is vital for efficient brain function. In the berry family, the Acai berry has the highest antioxidant level which makes them a super brain food.

The cacao bean is also being reported by some of the top health experts as the most exciting health food. Unfortunately, the benefits of the cacao bean are not as powerful in the form of a chocolate bar or Americans would be a lot healthier! The beans must be consumed after minimal processing. Ingesting a 1000% organic powder form of cacao is the best way to experience its wonderful benefits for the brain. It is probable that more in depth research will lead to an increase in organic, minimally processed cacao products that can be found in the marketplace.

As one can see, although the blueberry is quite popular among fruits, it is not the only fruit that positively affects the brain. In reference to the previously discussed blueberry study, patients who added blueberries to their daily diet over a period of 12 weeks noticed improvements in their mental function, specifically spatial working memory, in as little as 3 weeks. The additional good news about blueberries is that besides the benefits it provides for memory function, you can enjoy this healthy snack daily and your entire body will reap the benefits of its antioxidants. The researchers from the Peninsula Medical School and the University of Reading plan on performing future studies involving Alzheimer’s patients and the effect that flavonoid rich foods have on memory impairment. It is the hope of many researchers that they can unlock a secret that will lead to more effective treatments for Alzheimer’s patients and slow the progression of the disease.

Reference

WILLIAMS, C., ELMOHSEN, M., VAUZOUR, D., RENDEIRO, C., BUTLER, L., ELLIS, J., WHITEMAN, M., SPENCER, J. (2008). Blueberry-induced changes in spatial working memory correlate with changes in hippocampal CREB phosphorylation and brain-derived neurotrophic factor (BDNF) levels. Free Radical Biology and Medicine DOI: 10.1016/j.freeradbiomed.2008.04.008

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Adult Attention Deficit Disorder: A Real Concern http://brainblogger.com/2008/05/16/adult-attention-deficit-disorder-a-real-concern/ http://brainblogger.com/2008/05/16/adult-attention-deficit-disorder-a-real-concern/#comments Fri, 16 May 2008 15:16:38 +0000 http://brainblogger.com/?p=890 Psychiatry and Psychology CategoryAdult attention deficit disorder or AADD is characterized as a condition causing inattentiveness, organization problems, procrastination and difficulty completing work. It is believed that adults can see an onset of AADD later in life maybe as a carryover from childhood, but in order to receive a diagnosis you must have had symptoms as a child. The condition has differing levels of severity so treatment options vary all the way from coping skills to medication to control the symptoms. Medical intervention will come with some unwanted side effects so many patients opt for social counseling and other less invasive treatment options.

FocusADHD or attention deficit hyperactivity disorder is similar to AADD but research has shown that one third of the adults affected with AADD do not show any hyperactive behavior. Thus, the medical community has taken to using the AADD term instead.

In the brain of patients with AADD, executive function is impaired. This is the function that governs a person’s ability to monitor their own behavior by organizing and planning. This disorder affects approximately 2 to 4% of adults.

AADD patients are often the types seen by others as not thinking before they speak or act. They are sometimes referred to as a Type A personality or an always on the go individual. While they may seem to be driven, it is noted that they are rarely focused on one task long enough to see it to completion. In a recent study, three different groups of AADD patients all scored much lower than non-AADD adults on a dual memory and simultaneous capacity test, demonstrating their inability to concentrate in such situations. While this may seems like a small step, this recognition helps prove AADD to be a real concern.

As mentioned, treatment options vary depending on the severity of symptoms. For some AADD patients the symptoms are bad enough that medications along with social therapy are prescribed. Some of the more popular prescription medications are Ritalin, Adderall or Vyvanse. Ritalin is the most commonly known medication and is used in the treatment of ADD in children with some success. Adderall is a psychostimulant and Vyvanse (also used for children) is a stimulant as well.

It may seem strange that stimulants are prescribed for a disorder that sometimes causes hyperactivity but they are effective in many cases. This is thought to be accomplished by coaxing the brain to manufacture more serotonin. Increased serotonin has been shown to have a calming effect. This not only treats the hyperactive symptoms but may allow an adult to focus on their tasks at hand and see them to completion.

As recognition of AADD grows, more studies may lead to new treatments and an increased awareness of the disorder.

Reference

Dige, N., Maahr, E., Backenroth-Ohsako, G. (2008). Memory Tests in Subgroups of Adult Attention Deficit Hyperactivity Disorder Reveals Simultaneous Capacity Deficit. International Journal of Neuroscience, 118(4), 569-591. DOI: 10.1080/00207450701239384

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Cell Transplants for Parkinson’s Disease http://brainblogger.com/2008/05/12/cell-transplants-for-parkinsons/ http://brainblogger.com/2008/05/12/cell-transplants-for-parkinsons/#comments Mon, 12 May 2008 14:04:12 +0000 http://brainblogger.com/?p=937 Neuroscience and Neurology CategoryParkinson’s disease is a disorder that affects the central nervous system and causes an impairment of speech and motor skills. Parkinson’s disease affects 1 in 100 people that are over 60 years of age and has a nearly equal incidence rate in women and men. It is second only to Alzheimer’s disease as the most common neurodegenerative disease. Five to ten percent of Parkinson’s patients have an early onset around the age of 40 or younger.

Parkinson’s disease develops as the result of nerve cell damage or death in the midbrain. The cells that are impaired are responsible for the production of dopamine, this neurotransmitter aids in the transmission of signals from the midbrain to the corpus striatum. The proper transmission of these signals is needed for coordinated movement. Currently, treatment options for Parkinson’s include medications such as L-dopa to treat individual symptoms like stiffness and tremors. There is also an entire class of L-dopa derivatives that perform similar functions and are more efficiently converted into dopamine in the body. Unfortunately, the L-dopa derivatives cause more negative side effects than the traditional L-dopa drugs. In addition, each Parkinson’s case is unique to the patient and the severity of symptoms often varies considerably from patient to patient so treatment must be tailored to each individual.

Glial cellsA study published recently in the journal Glia discusses an exciting discovery of “radial glia-like cells” that lead to the production of dopaminergic neurons in the midbrain. These are the neurons typically affected by Parkinson’s disease. Glial cells nourish, protect, and support neurons. Researchers hope that this discovery may lead to a scientific method that would allow them to artificially reproduce dopaminergic neurons. The transplantation of healthy radial glia-like cells into the brain of Parkinson’s patients may lead to the regeneration of dopaminergic neurons that were damaged or destroyed.

Another study recently published in Nature Medicine showed that in some patients the progression of Parkinson’s disease can affect transplanted dopaminergic neurons that were grafted into an individual’s brain up to one decade earlier. As previously stated, each Parkinson’s case is unique. Some patients may continue to respond positively to the dopaminergic neuron grafts after prolonged periods of time while in other patients the disease will begin to affect the transplanted cells after one decade. Despite this discovery, the benefits of dopaminergic neuron transplantation are quite evident. After a successful transplantation patients usually experience reduced rigidity and an increase in the speed at which they can move. Researchers hope that figuring out why transplanted neurons can be affected in Parkinson’s patients will identify the mechanism of the disease. A better understanding of how this disease develops can lead to treatments that slow or prevent the progression of symptoms.

In conclusion, the contradictory results from these two studies suggest that more research regarding the development and progression of this disease needs to be the focus of treatment. More specifically, discovering how the disease can affect healthy transplanted neurons that were cultured in a clinical setting will undoubtedly lead to the control and prevention of this disease. These types of discoveries may also lead to a better quality of life for Parkinson’s patients.

References

Bonilla, S., Hall, A.C., Pinto, L., Attardo, A., Gotz, M., Huttner, W.B., Arenas, E. (2008). Identification of midbrain floor plate radial glia-like cells as dopaminergic progenitors. Glia, 56(8), 809-820. DOI: 10.1002/glia.20654

Li, J., Englund, E., Holton, J.L., Soulet, D., Hagell, P., Lees, A.J., Lashley, T., Quinn, N.P., Rehncrona, S., Bjorklund, A., Widner, H., Revesz, T., Lindvall, O., Brundin, P. (2008). Lewy bodies in grafted neurons in subjects with Parkinson’s disease suggest host-to-graft disease propagation. Nature Medicine, 14(5), 501-503. DOI: 10.1038/nm1746

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Generalized Anxiety Disorder: The Mind/Body Connection http://brainblogger.com/2008/05/05/gad-the-mindbody-connection/ http://brainblogger.com/2008/05/05/gad-the-mindbody-connection/#comments Mon, 05 May 2008 14:16:31 +0000 http://brainblogger.com/?p=894 BioPsychoSocial Health CategoryGAD or generalized anxiety disorder is defined as a disorder characterized by irrational, uncontrollable worry about everyday issues and events. While someone without GAD may find themselves anxious in certain scenarios, persons with GAD may be almost paralyzed with anxiety in situations that should not generate that level of fear and worry. This anxiety may manifest itself physically through hot flashes, an accelerated heart beat, sweating, muscle aches, irritability and health issues.

While it has long been known that GAD can affect someone physically, new research is pointing to potential causes for GAD. Reported in Archives of Internal Medicine, researchers are studying the effects of some conditions such as thyroid disease, arthritis, migraine and respiratory disease and their connection to the onset of GAD. They approached this study knowing that physical illness often leads to depression. They wanted to find out if physical illness may cause GAD or other anxiety disorders.

PhobiaThey studied more than 4,000 adults for two years for signs of the GAD mind/body connection. They included all anxiety disorders such as agoraphobia, obsessive-compulsive disorder and panic disorder. Their results thus far show an increased rate of anxiety disorders in patients suffering from physical conditions. They are trying to figure out how and why the connection exists. One thought is that when a person is suffering a physical illness they are faced with increased worry and anxiety, triggering the development GAD.

I would go one step further to say that it seems like the brain gets “stuck” in the worry and anxiety mode, and maybe it can’t get out of it due to the existing stress on the body caused by the illness. It would be interesting to see if GAD patients without illness triggers can recover from their GAD more easily.

It is the hope of researchers that these studies will have the same effect on the medical community as the depression/physical illness studies. As more was learned about depression and physical illness, more doctors watched for the signs in their patients and made treatments available. There may come a day when physical illness automatically leads to a mental health evaluation to help patients circumvent depression and anxiety.

Some doctors may begin to screen for GAD and prescribe antidepressant or anti-anxiety medication for conditions shown most likely to induce depression or anxiety disorders. In some cases this may be handled in a proactive manner if a patient is already an anxious or depressive person.

Reference

Sareen, J., Jacobi, F., Cox, B.J., Belik, S., Clara, I., Stein, M.B. (2006). Disability and Poor Quality of Life Associated With Comorbid Anxiety Disorders and Physical Conditions. Archives of Internal Medicine, 166(19), 2109-2116. DOI: 10.1001/archinte.166.19.2109

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Preteens Feel the Effects of Mom’s Pregnancy Bad Habits http://brainblogger.com/2008/04/20/preteens-feel-the-effects-of-moms-pregnancy-bad-habits/ http://brainblogger.com/2008/04/20/preteens-feel-the-effects-of-moms-pregnancy-bad-habits/#comments Sun, 20 Apr 2008 14:11:59 +0000 http://brainblogger.com/?p=872 Neuroscience_Neurology2.jpgIt has been known for years that babies in utero (womb) suffer ill effects from their mothers’ exposure to tobacco, drugs and alcohol. A new study funded by the National Institute on Drug Abuse and performed by Michael Rivkin of Children’s Hospital Boston showed that children exposed to these toxins may suffer effects well into early adolescence.

Using MRI technology, the study looked into the long term effects of prenatal exposure to drugs, alcohol, tobacco or a combination of the three on the brain structure of preteens. The study found that these kids have thinner cortical grey matter than subjects who did not suffer exposure to toxins in utero. This study also showed a reduction in brain volume directly tied to this exposure.

BabyThere have been many studies pointing to the long term effects of alcohol on babies in utero but generally these types of studies have only looked at children suffering from Fetal Alcohol Syndrome. There is a lack of studies on children who were not diagnosed with Fetal Alcohol Syndrome but may be affected by even their limited prenatal alcohol intake. There is continuing research into the many effects of prenatal alcohol use.

Fetal Alcohol Spectrum Disorder, which is the diagnosis for these affected preteens, is not itself a disease but is a group of symptoms. The neurological effects can range from mild to very serious. The symptoms include everything from epilepsy, seizure disorders, hearing loss, clumsiness, poor gait, and impaired fine motor skills and hand-eye coordination. It also may cause another related disorder called Sensory Integration Disorder or SID.

MRISID is defined as a neurological disorder that interferes with the information processing related to the five senses: taste, hearing, touch, smell and sight. This causes the brain to perceive information from the body abnormally. This often causes hyper- and hypo-sensitivities in affected children. An example of hyper-sensitivity is the inability to tolerate touch or even the feel of clothes against the skin. Conversely, hypo-sensitivity can make a child very restless and in constant need of stimulation.

There is no doubt that more studies will continue to find these types of brain disorders in children exposed to alcohol, drugs and/or tobacco in utero. It would not be surprising to find that these effects may stay with these children for their entire lifetime. It is the hope of most researchers that this information will lead to better education programs for pregnant women.

Reference

Rivkin, M.J., Davis, P.E., Lemaster, J.L., Cabral, H.J., Warfield, S.K., Mulkern, R.V., Robson, C.D., Rose-Jacobs, R., Frank, D.A. (2008). Volumetric MRI Study of Brain in Children With Intrauterine Exposure to Cocaine, Alcohol, Tobacco, and Marijuana. Pediatrics, 121(4), 741-750. DOI: 10.1542/peds.2007-1399

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The Timing of Plaque Formation is a Critical Factor in Alzheimer’s Dementia http://brainblogger.com/2008/04/14/the-timing-of-plaque-formation-is-a-critical-factor-in-alzheimers-dementia/ http://brainblogger.com/2008/04/14/the-timing-of-plaque-formation-is-a-critical-factor-in-alzheimers-dementia/#comments Tue, 15 Apr 2008 05:00:20 +0000 http://brainblogger.com/?p=818 Neuroscience_Neurology.jpgResearchers at the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND) and Washington University School of Medicine have recently shifted their focus of Alzheimer’s disease (AD) research from understanding the role that plaques and other neurological changes play in the progression of AD. Now they are looking at the time period and order in which plaques and neurological changes like dementia and senility occur in the progression of AD.

SynapseAD is a neurodegenerative disorder that is classified based on the formation of neuritic amyloid plaques (clusters of dead or dying neuronal cells), neurofibrillary tangles (abnormally twisted protein fragments), dementia and senility. The loss of neuronal and synaptic function in certain parts of the brain has been associated with dementia and memory loss in AD patients. Neuronal and synaptic processes regulate the brain’s electrical and chemical signaling system so damage to neuronal and synaptic connections can cause severe cognitive and speech impairment. AD is progressive and usually starts to present itself between the ages of 40 and 50. The first symptom is typically memory loss; shortly thereafter the individual may develop speech and cognitive problems.

Researchers at Washington University and MGH-MIND used a novel microscopic imaging procedure to analyze the time period of neurological changes in transgenic mice they knew would develop amyloid plaques. The research groups began their studies by regularly (weekly and daily) imaging plaque-free regions in the brain of mice. In some cases, plaques appeared 24 hours after an image showing no plaques was obtained. When images from mice were compared to that of individuals with AD, the plaques that developed in the mice were similar to that of plaques that typically develop in AD patients. Further analysis of the mice that developed plaques showed that once the plaques formed, the size did not significantly change.

The development of amyloid plaques has for some time now been associated with an increase in the number of microglial cells in the brain of AD patients. Microglia are immune cells that are stimulated by neuronal inflammation or damage. This mouse model included the expression of a fluorescent microglial marker, which showed that microglial cells migrated towards new plaques within 1 day of their development. To date, whether microglia breakdown plaques or prevent further plaque formation is not clear. This study also showed that neurological degeneration caused by plaques hindered normal electrical signaling between adjacent neurons and led to physical AD symptoms approximately five days after the appearance of the plaques.

Protein (GABA-R)The results of this study showed that the formation of plaques are the initial factor that causes neurological changes like dementia and the loss of cognitive function in AD patients. Groups who study AD at various institutions have begun to analyze the expression of proteins that are directly associated with plaque formation. One such protein, called A beta N3(pE), is shorter than the normal A beta protein, has an increased toxicity in comparison to the normal A beta protein, and has an increased aggregation rate. This type of research in combination with recent results that label plaque formation as the primary cause of Alzheimer dementia are currently causing a shift in the focus of AD treatment to the inhibition of plaque formation. This MGH-MIND research project was published in Nature.

Reference

Meyer-Luehmann, M., Spires-Jones, T.L., Prada, C., Garcia-Alloza, M., de Calignon, A., Rozkalne, A., Koenigsknecht-Talboo, J., Holtzman, D.M., Bacskai, B.J., Hyman, B.T. (2008). Rapid appearance and local toxicity of amyloid plaques in a mouse model of Alzheimer’s disease. Nature, 451(7179), 720-724. DOI: 10.1038/nature06616

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New Anti-Cancer Drug for Aggressive Brain Tumors http://brainblogger.com/2008/04/01/new_anti_cancer_drug_for_aggressive_brain_tumors/ http://brainblogger.com/2008/04/01/new_anti_cancer_drug_for_aggressive_brain_tumors/#respond Tue, 01 Apr 2008 19:29:49 +0000 http://brainblogger.com/?p=819 Drugs_Clinical_Trials2.jpgResearchers are constantly trying to find new drugs or forms of therapy that can be used to treat cancer. Quite often when a possible treatment is discovered, being allowed to test a drug or other experimental cancer treatment at a clinical level is difficult. For example, after an anti-carcinogenic drug has been thoroughly tested at the experimental level it is necessary to test it in humans to analyze factors such as the drug’s anti-tumor activity, its ability to interact with a specific target, and to discover which patients are more likely to benefit from the drug. These types of early clinical trials are the key in the successful implementation of effective anti-tumor drugs and therapies.

One such study was done to treat a small group of glioblastoma patients with an experimental drug called rapamycin since they needed to undergo surgery because their glioblastoma tumors returned. Glioblastomas are aggressive brain tumors that are very invasive and exhibit rapid metastasis. Currently chemotherapy and surgery are not effective treatments for this type of cancer and in most cases, the tumors often return after treatment. This has caused researchers to look for alternative forms of treatment for glioblastomas that include anti-tumor drugs. An interesting discovery about glioblastoma cases is that approximately 40% of patients who develop glioblastomas have a gene called PTEN that becomes inactive. PTEN is a tumor suppressor gene that sensitizes cancer cells to drugs called mTOR inhibitors when it is inactivated. mTOR is a protein that plays a role in cell growth and proliferation. Rapamycin, also called Sirolimus, is an mTOR inhibitor and the anti-carcinogenic and well as immunosuppressive affects of these types of drugs are currently being evaluated.

For this study, 15 patients whose glioblastoma tumors returned were treated with different amounts of rapamycin one week before and after surgery. Each of these patients had tumors that did not express the PTEN gene and if the tumor appeared to be progressing after surgery the rapamycin treatment was discontinued. The purpose of this study was to determine if the drug could inhibit tumor growth and if so, at what concentration. In addition the researchers were hoping to reveal which patients were more likely to respond to rapamycin treatment.

The results of this study showed that the rate of tumor cell proliferation decreased in 7 of the 15 patients treated with rapamycin after surgery, and severe toxicity did not occur in most of the patients. The reduction of tumor cell proliferation was directly correlated to the inhibition of the mTOR protein. Scans that were obtained from 2 patients even showed signs that the tumor mass was decreasing. Unfortunately, when tumor cells that reacted to rapamycin in patients were tested in a laboratory setting, the cells no longer responded to rapamycin treatment. This appeared to be due to the drug’s inability to penetrate the tumor ex vivo. In addition, the treatment of rapamycin led to the activation of a protein called Akt in some patients, which decreased the time period between surgery and a reoccurrence of their tumor.

These results showed that although rapamycin caused a reduction of tumor cell proliferation in some glioblastoma patients, in others it activated a second protein that accelerated the progression of the disease. This strengthens the point that these types of studies are essential. The side effects of this drug in some patients is life threatening so it is important to analyze the clinical effects from a small group of selected patients before the drug is distributed on a large scale level or in clinics nationwide.

Reference

Cloughesy, T.F., Yoshimoto, K., Nghiemphu, P., Brown, K., Dang, J., Zhu, S., Hsueh, T., Chen, Y., Wang, W., Youngkin, D., Liau, L., Martin, N., Becker, D., Bergsneider, M., Lai, A., Green, R., Oglesby, T., Koleto, M., Trent, J., Horvath, S., Mischel, P.S., Mellinghoff, I.K., Sawyers, C.L. (2008). Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma. PLoS Medicine, 5(1), e8. DOI: 10.1371/journal.pmed.0050008

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Magnetoencephalography: A Breakthrough Imaging Technique for Pediatrics http://brainblogger.com/2008/03/10/magnetoencephalography-a-breakthrough-imaging-technique-for-pediatrics/ http://brainblogger.com/2008/03/10/magnetoencephalography-a-breakthrough-imaging-technique-for-pediatrics/#comments Mon, 10 Mar 2008 16:08:42 +0000 http://brainblogger.com/2008/03/10/magnetoencephalography-a-breakthrough-imaging-technique-for-pediatrics/ Neuroscience_Neurology2.jpgMagnetoencephalography (MEG) is an imaging technique that is currently being used before resective surgery in pediatric epilepsy patients to determine whether or not surgery is necessary and if the surgery will be successful. Before this technique was implemented, doctors had to rely on symptoms caused by seizures and traditional techniques that did not provide sufficient information about the success or possible long-term, adverse effects of resective surgery.

Epilepsy affects 1 in 1,000 children every year. Children who suffer from epilepsy are usually prescribed antiepileptic medication to control frequent seizures and have an increased mortality rate due to factors that include neurological deterioration. When medication is not a sufficient treatment for epilepsy, surgery is often required. In the past, surgery was only considered for severe epilepsy cases, but today pediatricians choose resective surgery to treat epileptic children as a means of avoiding long-term consumption of antiepileptic medication. Surgery is also considered for cases where frequent seizures begin to hinder a child’s development or cause encephalopathy (cerebral inflammation).

MEG is a promising technique for the treatment of uncontrollable epilepsy in pediatric patients because it provides noninvasive analysis of the ictal onset zones (IOZ), which are the regions of seizure onset and the functional cortex (motor, sensory, and language regions). A MEG can be used to detect abnormal interictal (period between seizures) brain activity and is particularly useful for locating anatomic lesions that could not be detected by techniques like thin section magnetic resonance imaging (MRI).

Researchers at the Children’s Hospital of Philadelphia recently evaluated the accuracy at which the IOZ and functional cortex could be located by comparing the MEG technique to traditional techniques such as ictal electroencephalography (EEG), interictal EEG, magnetic resonance imaging (MRI), functional cortical mapping, neuropsychological examinations, nuclear imaging, the Wada procedure, and the analysis of clinical seizure symptoms. The results of their evaluation showed that a MEG plays 4 vital roles in the detection of ictal onset zones and the functional cortex:

  • The use of a MEG to accurately detect the zones of interest removes the need for long-term intracranial EEG monitoring during epilepsy surgery.
  • From a MEG, a doctor can detect bilateral, multifocal, and diffuse ictal onset zones, showing that the pediatric patient should not undergo resective surgery.
  • A MEG provides more accurate localization and therefore allows the doctor to make a concrete decision about resective surgery, compared to traditional methods that normally only suggest multifocal ictal activity.
  • A MEG allows doctors to locate the eloquent cortex, which is the region of the brain that if removed, causes a loss of sensory and/or linguistic skills. This is an important factor in determining if surgery is required and can be used to avoid damaging this region during resective surgery.

In the future, a MEG may also be used to make decisions such as whether or not surgical procedures like intracranial grid placement or guiding electrode placement are necessary in addition to the detection of lesions that are normally undetectable.

Currently neuroradiologists, neurologists, neurosurgeons, neuropsychologists, and physicists are among the groups of physicians that are involved in guaranteeing that the implementation of MEG for pediatric epileptics is a safe procedure that will allow physicians to more accurately determine which pediatric patients will benefit from resective surgery.

Reference

Schwartz, E., Dlugos, D., Storm, P., Dell, J., Magee, R., Flynn, T., Zarnow, D., Zimmerman, R., Roberts, T. (2008). Magnetoencephalography for Pediatric Epilepsy: How We Do It. American Journal of Neuroradiology. DOI: 10.3174/ajnr.A1029

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New MRI Opens New Doors http://brainblogger.com/2008/02/23/new-mri-opens-new-doors/ http://brainblogger.com/2008/02/23/new-mri-opens-new-doors/#comments Sat, 23 Feb 2008 12:28:10 +0000 http://brainblogger.com/2008/02/23/new-mri-opens-new-doors/ Neuroscience_Neurology2.jpgMagnetic Resonance Imaging (MRI) is an important imaging technique used in the medical field to diagnose many diseases and detect abnormalities in the human body non-invasively. In the neurological sense, an MRI is often performed to obtain an inner image of the brain if unusual activity is suspected. For example in the case of multiple sclerosis (MS), abnormal spots called lesions can be detected with an MRI before clinical symptoms occur. MRIs have advantages over other imaging methods because this system is thorough and can be used to detect small subtle changes during the early stages of diseases. One limitation is that the scans usually take several hours to complete.

Now, thanks to dedicated researchers at the University of Illinois in Chicago, the world’s most powerful MRI is ready to be used to help the first patient. The team’s machine received final approval from the Food and Drug Administration (FDA) in the cusp of the 2008 new year. With an entire journal article solely dedicated to the safety of the machine in the Journal of Magnetic Resonance Imaging, the 9.4 Tesla machine will open up a new field in medical imaging, particularly neurology.

Typical clinical MRI scanners have magnetic field strengths of 0.2 to 3 Tesla. At these strengths only the movement of water molecules can be visualized, which limits the observation of metabolic processes in the brain to abnormal cystic or tumor formations and abnormalities in blood vessels or the heart. In 2003 MRIs with magnetic field strengths as high as 8 Tesla were accepted by the FDA, but to date, the 9.4 Tesla scanner is the most powerful clinical scanner that is large enough to acquire images from the human brain.

The 9.4 Tesla MRI allows doctors to visualize molecules other than water. For example, doctors will now be able to perform sodium imaging to determine whether a brain tumor is shrinking, growing, or migrating all in one visit. Previous MRI scanning required that the patient make several trips to the hospital over a period of weeks and sometimes even months. The reason that only one visit is necessary with the 9.4 Tesla scanner is that this high magnetic field strength allows more molecules to be visualized in a shorter period of time in comparison to the lower strength scanners that are currently being used. Imaging technology is now moving towards patient studies such as sodium imaging and towards safety testing for oxygen and phosphorus imaging in humans. Researchers are hoping that this scope can even be extended to other, more rare molecules in the future.

Analyzing a patient’s metabolic pattern after the administration of a therapeutic agent will allow doctors to customize treatment plans as well as determine the optimal type and amount of drugs to prescribe their patients. There are no known harmful side effects of undergoing an MRI besides the exposure to magnetic fields which should be avoided during pregnancy. Patients undergoing an MRI procedure sometimes experience mild nausea or claustrophobia from being inside of a chamber.

Currently MRI is the preferred imaging technique in diagnosing and monitoring diseases such as stroke, tumors, blood vessel abnormalities, infections, Multiple Sclerosis, and many other neurological and non-neurological diseases.

Reference

University of Illinois at Chicago (2008) World’s Most Powerful MRI Ready To Scan Human Brain. ScienceDaily.

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Eat Less, Live Longer: By Diet or Drugs http://brainblogger.com/2008/02/13/eat-less-live-longer-by-diet-or-drugs/ http://brainblogger.com/2008/02/13/eat-less-live-longer-by-diet-or-drugs/#comments Wed, 13 Feb 2008 18:35:55 +0000 http://brainblogger.com/2008/02/13/eat-less-live-longer-by-diet-or-drugs/ Articles_Studies.jpgFor years, studies have shown that an almost foolproof way to live longer is to cut back on calories. In mice, cutting calories has not only extended their lifespan, but also their reproductive period. It is hypothesized that a low calorie diet in humans can have a similar effect.

In yeast, it was demonstrated that decreasing caloric intake of these cells decreases SIR2, an inhibitor of an anti-aging enzyme. Lower production of SIR2 meant the longevity system of the cell flourished. We humans have similar genes, and it is likely it is modulated in a similar manner.

We already know that cutting back on calories can lower cholesterol, fasting glucose, and blood pressure. These parameters have also been termed biomarkers of aging, as they can be correlated with age related diseases.

Don’t want to cut back on your gastronomic experiences? Then pop an antidepressant. Unlike Prozac or Zoloft, when worms were given another anti-depressant called mianserin (trade name Tolvon), their appetite center was tricked into thinking they had consumed much less calories than they actually did. Their lifespan was increased significantly, from 3 weeks to more than four.

According to Linda Buck, Nobel Prize winner and leader of this study, the drug works by modulating neurotransmitter serotonin, which controls appetite and hunger sensation in both these worms as well as in humans. It also stimulates octopamine, which is a trigger for starvation. While the worm’s nervous system was tricked into thinking they were starving, the organisms did not consume less food. Furthermore, when the worms were put on a diet on top of the antidepressant treatment, there was no additional increase in lifespan beyond the basal effect of a caloric cutback. This suggests that mianserin uses the exact same mechanism as a strict diet to make the worms live longer.

While these findings have yet to be shown in humans, we see ample evidence that diet does have a similar effect in us. For example, inhabitants of the Ryukyu Islands of Japan have the highest life expectancy. These people consume a low calorie diet which is positively correlated with the number of people living over the age of 110.

References

  • Lin, S. Genes & Development, 18, (2004)
  • Petrascheck, M. et al. Nature 450, 553-557 (2007)
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Diabetes Protects Against Migraines http://brainblogger.com/2008/02/07/diabetes-protects-against-migraines/ http://brainblogger.com/2008/02/07/diabetes-protects-against-migraines/#comments Thu, 07 Feb 2008 19:35:58 +0000 http://brainblogger.com/2008/02/07/diabetes-protects-against-migraines/ Researchers are grappling with findings that people living with diabetes are less likely to have migraines, and vice versa. While the data has been made public about populations in several regions for quite some time now, for the first time a series of systematic studies and reviews conclude that these findings are not just a fluke. An entire region in Norway was sent a questionnaire. The 1,499 people who self reported to be living with any form of diabetes were found to have a significantly lower rate of migraines than those reporting to be non-diabetics.

There was no positive or negative correlation between non-migraine headaches and diabetes mellitus, nor was there any skewed correlation with age. Very few in this population were living with both migraines and diabetes mellitus.

There is still no hard evidence pointing towards why or how the two diseases are inversely correlated with one another. Diabetes mellitus is a disease which affects glucose absorption of the body, while migraines are known to be caused by vascular perturbations in the brain. However, it is thought that the blood vessel properties change in diabetes patients, thus making it possible to somehow protect the brain against these vessel-induced headaches. More research needs to be done to support this theory.

This is not the first time an inverse relationship between two seemingly unrelated diseases has been demonstrated. Canadian neurologist Patrick McGeer has shown in 1991 that there was a 5 times less likelihood of someone living with rheumatoid arthritis (RA) to get Alzheimer’s Disease. Here, autoimmune RA clearly plays some unknown protective role against later on developing a senile neuroinflammatory disorder.

While these findings at first glance seem peculiar, they may shed light into our hazy understanding of these diseases. Furthermore, knowing exactly how one disease protects against another may prompt researchers to mimic this effect through a therapeutic treatment.

References

H. Aamodt, L. J. Stovner, K. Midthjell, K. Hagen, J.-A. Zwart (2007) Headache prevalence related to diabetes mellitus. The Head-HUNT Study. European Journal of Neurology 14 (7), 738–744.

Jenkinson ML, Bliss MR, Brain AT, Scott DL. (1989) Rheumatoid arthritis and senile dementia of the Alzheimer’s type. Br J Rheumatol 8:86-8.

McGeer PL, McGeer E, Rogers J, Sibley J. (1990) Anti-inflammatory drugs and Alzheimer’s disease. Lancet 335:1037.

Beard CM, Kokman E, Kurland LT. (1991) Rheumatoid arthritis and susceptibility to Alzheimer’s disease. Lancet 37:1426.

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Multiple Sclerosis (MS) Linked to Genes http://brainblogger.com/2008/01/26/multiple-sclerosis-ms-linked-to-genes/ http://brainblogger.com/2008/01/26/multiple-sclerosis-ms-linked-to-genes/#comments Sat, 26 Jan 2008 14:21:09 +0000 http://brainblogger.com/2008/01/26/multiple-sclerosis-ms-linked-to-genes/ Neuroscience and Neurology CategoryScientists have recently pinpointed genes that can predict who is more likely to get Multiple Sclerosis (MS). MS is thought to be an autoimmune disease, meaning the body attacks itself, and to date it affects approximately 400,000 Americans. Every week about 200 people are diagnosed with this potentially debilitating disease in the US alone. Although the most common image of MS is an elderly individual in a wheelchair, the first signs of disease (periods of dizziness, double vision) often appear in the late teens or early twenties, and twice as often in women. The patient may recover completely, partially, or not at all after this first “relapse” episode, and it is a lifelong disease. Most MS patients will get some permanent disability later on in their lives.

MS is a disease for which we have no cure, because scientists know very little about what causes it. Current treatment options can only modulate the disease or lessen the symptoms. There are generally two streams of thought in the scientific community on what causes the disease: it is either thought to be triggered by the environment, or it is thought that there is a genetic predisposition. Many scientists also propose both factors play a role, given the current evidence. For instance, in Japan, the adoption of a “Western” lifestyle starting in the 1950s has been correlated with a dramatic increase in the incidence of MS. Also, there are statistics showing that the further away from the equator, the higher the incidence rate of MS. It has even been proposed that Vitamin D, which our body produces with the help of sunlight, plays a protective role against MS. It would make sense then, that the sun-intensive equator regions would have a lower incidence of the disease.

Nevertheless, it is now known that genes do play an important role in predicting MS as well. A study spearheaded by researchers from Duke University have found that an important marker in the development and programming of the immune system called the Interleukin 7 alpha receptor (IL-7RA) strongly correlates with MS disease susceptibility. It is now being investigated whether this marker plays a role in causing the disease, providing a valuable clue as to how and why certain people get this illness. Despite the fact that much more research needs to be done, the study provides strong evidence that genetics are an important component, and point the research community in a helpful direction in finding a cure for the disease.

References

Gregory S et al. IL 7 Receptor alpha chain shows allelic and functional association with multiple sclerosis. Nature Genetics 2007 Sept, 39(9):1083-90.

Broadley SA. Could vitamin D be the answer to multiple sclerosis? Multiple Sclerosis 2007 Aug;13(7):825-6.

Kira J. Multiple sclerosis in the Japanese population. Lancet Neurology 2003 Feb;2(2):117-27. Review

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Our Caveman Way of Avoiding Danger http://brainblogger.com/2008/01/25/our-caveman-way-of-avoiding-danger/ http://brainblogger.com/2008/01/25/our-caveman-way-of-avoiding-danger/#comments Fri, 25 Jan 2008 14:25:04 +0000 http://brainblogger.com/2008/01/25/our-caveman-way-of-avoiding-danger/ Psychiatry_Psychology.jpgYou know the scenario. You are standing at a family get together lost in thought about a stressful situation in your life when a family member approaches and with a worried tone asks, “What’s wrong?” Did you know that subconsciously they are reading the facial signals you are displaying? Why don’t they have the same reaction when your mood is happy? Well, there is an evolutionary reason. A study looking at this phenomenon showed that we recognize fear on others’ faces faster than we notice happiness.

Researchers at Vanderbilt University in Tennessee studied the effect of perception when it applies to reading emotion on faces. Their study was published in the APA journal Emotion. Using a trick to slow down perception times, they found that there was a measurable difference in the amount of time it takes to perceive a happy face and a scared face, such that a scared face is recognized faster. This is probably due to the shape of the eyes, as this visual clue travels faster through the human brain. The researchers’ theory is that this is a natural occurrence as it was needed millions of years ago as a type of “threat radar.” This was and is used to signal other people that something is wrong and they need to pay attention.

Since our brains respond more to fear than other emotion it is easy to see why we respond more quickly when we see a loved one with a worried or fearful look. This is as important of an evolutionary response now as it was then, just not always for the same reasons. We probably won’t face the same threats as our ancestors but it is can still be a helpful tool for avoiding disaster and harm. The best lesson to be learned is that when you see a friend or a loved one and you think they look worried and fearful you should listen to your instinct. If someone is looking at you and they suddenly look over your shoulder with a look of fear, look around! Your gut feel is probably right and you are using millions of years of signals hardwired into your brain.

We should all appreciate the evolutionary gifts we have received as they all serve a purpose. Maybe not the purpose they served for the cavemen but we can still apply these gifts today to look out for each other. One lesson we can all take away from this study is that often what we feel is all over our face for everyone to see.

References

Yang, Eunice; Zald, David H.; Blake, Randolph. Fearful expressions gain preferential access to awareness during continuous flash suppression. Emotion. 2007 Nov Vol 7(4) 882-886

Cressey, Daniel. Fear gets seen faster. The Great Beyond (a Nature blog). 2007.

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Heart Chocolate – Friend or Foe? http://brainblogger.com/2008/01/20/heart-chocolate-friend-or-foe/ http://brainblogger.com/2008/01/20/heart-chocolate-friend-or-foe/#comments Sun, 20 Jan 2008 16:40:09 +0000 http://brainblogger.com/2008/01/20/heart-chocolate-friend-or-foe/ Alternative_Medicine.jpgThere is a new chocolate bar on the market called “Heart Chocolate” that claims to lower blood sugar and cholesterol. The secret behind this healthy chocolate is said to be a mixture of bitter melon and cinnamon (CM-X). Supposedly if you eat three portions throughout the day it controls your cravings while benefiting your cardiovascular system with the anti-inflammatory properties in the chocolate. Sounds like a ridiculously big claim for a sixty calories chocolate bar! The makers also claim that type-2 diabetics can eat it too since it is sugar free.

Bitter melon has been utilized for its pharmaceutical benefits since the 16th century offering patients a natural anti-bacterial, antiviral and anti-cancer treatment. In studies on animals, bitter melon has been shown to reduce cholesterol and triglycerides in modest amounts and reduce insulin resistance. Cinnamon has been used throughout history for the treatment of diabetes by traditional Chinese, Russian and Indian herbalists. OK, with all that said, can some bitter melon and cinnamon extracts really reduce cholesterol and blood sugar significantly? I really doubt it that they can put enough in a sixty calorie portion to have this effect without it tasting really bitter (because bitter melon isn’t called bitter for no reason).

There are a lot of problems with this product, aside from the fact that the FDA doesn’t regulate dietary supplements like this and therefore they claim whatever they want without having good science to back it up. It has been shown that artificial sweeteners actually contribute to the high blood sugar problems of diabetics through several mechanisms, so how can this chocolate bar with artificial sweeteners be lowering blood sugar levels. Sounds like a stretch to me.

My only hope is that the makers of this product are morally responsible enough to properly market this product as the dietary supplement that it is, rather than as a chocolate bar that anyone can eat. Unfortunately, supplements are often sold in the grocery stores amongst the other normal products on the shelf, like how “Smart Balance” is hidden in the butter section as if it is butter or margarine when really it is a supplement. So be on the lookout for this new heart supplement disguised as a chocolate bar next to your Milky Way and Mars bars!

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