Medicineworld.org: Archives of neurology news blog
Go Back to the main neurology news blog
Subscribe To Health Blog RSS Feed
Archives Of Neurology News Blog From Medicineworld.Org
Merry Christmas To All Our Readers
Oh, jingle bells, jingle bells
Jingle all the way
Oh, what fun it is to ride
In a one horse open sleigh
Jingle bells, jingle bells
Jingle all the way
Oh, what fun it is to ride
In a one horse open sleigh........
December 23, 2005
How Brain Replenishes Memory-making Molecules
Image credit: Credit: Pamela England, UCSFNew research on living neurons has clarified how the brain refreshes the supply of molecules it needs to make new memories.
The discovery by researchers at UCSF is reported today in the December 22 issue of the journal Neuron and is featured on the journal's cover.
Memory formation is thought to involve a strengthening of the communication between neurons in the part of the brain known as the hippocampus. Scientists know that this increased communication results from a surge in the number of receptors on one neuron that is available to bind to the neurotransmitter glutamate released from another neuron. The two neurons meet at a synapse.
But how and from where the brain gains fresh supplies of these crucial receptors has remained unclear. Known as AMPA receptors, they are essential for the rapid connections made between nerves during learning.
The researchers sought to answer this question by studying the basal trafficking of receptors -- the normal process by which receptors are replaced from fresh stores that are synthesized and located inside the cell. Focusing on live neurons cultured from rats, they discovered clear evidence to dispel the prevailing view that receptors at the synapse are constantly being replaced by stores inside the cell. Rather, the researchers found that the synaptic receptors are relatively stable, lasting about 16 hours before they are replaced.
The study also supports an unsuspected route by which new receptors make their way to the synapse: Fresh AMPA receptors appear to be placed on the cell surface at the cell body and then migrate along the arms or dendrites of the cell to synapses, rather than moving within the cell to the synapse as had been thought.
The researchers suspect the trafficking process their research revealed also occurs during learning and memory formation, but at a much faster rate. The study may provide insight into how to treat memory disorders, said Pam England, PhD, assistant professor of pharmaceutical chemistry at UCSF and senior author on the study.........
December 21, 2005
Pain and The Brain
With training and the use of high-tech imaging equipment, subjects were able to influence their pain by controlling activity in one of the pain centers of the brain through the use of mental exercises and by visualizing their own brain activity in real time.
Compare it to exercising your muscles in a top-of-the-line weight room. After repeated practice, you get better at it.
The researchers are hopeful the new technique may have potential for future use as long-term therapy for chronic pain patients-possibly even without all the high-tech equipment. They caution that significantly more work is needed before it can be thought of as a clinical therapy.
"We believe these subjects and patients really learned to control their brain and, through that, their pain," said Sean Mackey, MD, PhD, assistant professor of anesthesia and co-author of the study would be published in the Dec. 12 online issue of the Proceedings of the National Academy of Sciences.
The study posed two questions: "Can healthy subjects and patients with chronic pain learn to control activity in specific regions of their brain? And, in doing so, does this lead to an improved control of their pain?" The answer to both was a resounding "Yes." A second, larger study is under way to test the potential for long-term use in future treatment.
"Pain has a huge impact on individual patients, their families and society," said Mackey, who is also associate director of Stanford's pain management division. A recent national survey showed that more than half of all Americans suffer from chronic pain. "I got incredibly jazzed by the results [of the imaging study]," Mackey added. "We could change people's lives. However, significantly more science and testing must be done before this can be considered a therapy for chronic pain".........
December 21, 2005
Light-sensing cells in retina
The scientists report in the Dec. 22 issue of Neuron that in the mouse retina, intrinsically photosensitive retinal ganglion cells (ipRGCs) are active and functioning at birth. That was surprising because the mouse retina doesn't develop fully until a mouse is almost three weeks old, and the first rod cells don't appear until about 10 days after birth.
"We were stunned to find these photoreceptors were firing action potentials on the day of birth," says Russell N. Van Gelder, M.D., Ph.D., associate professor of ophthalmology and visual sciences and of molecular biology and pharmacology. "Mice are very immature when they're born. It takes about three weeks after birth for the retina to fully develop. No one previously had detected light-dependent cell firing in a mouse before 10 days."
Van Gelder says the ganglion cells react to light in two ways, sending messages to parts of the brain that control circadian rhythms, and (on the first day or two of life) also setting off a wave of activity that spreads through the retina, possibly helping visual cells develop.
Van Gelder and his colleagues have spent the last few years learning how blind animals (and people) can sense light and use it to set their circadian clocks. The ipRGCs were first identified in 2002 - by David M. Berson, Ph.D., and his colleagues at Brown University - as the cells that could sense light even in visually blind eyes. But it was very difficult and time consuming to isolate and study the cells, requiring precise injection of a tracing dye into the brains of animals to label and identify the ipRGCs.........
December 20, 2005
Sneaking Drugs Into The Brain
The brain is a complex organ with a number of different types of cells and structures, and it is fortified with a protective barrier erected by blood vessels and glial cells - the brain's structural building blocks - that effectively blocks the delivery of most drugs from the bloodstream.
But now researchers have found a new way to sneak drugs past the blood-brain barrier by engineering and implanting progenitor brain cells derived from stem cells to produce and deliver a critical growth factor that has already shown clinical promise for treating Parkinson's disease.
Writing today in the journal Gene Therapy, UW-Madison neuroscientist Clive Svendsen and colleagues describe experiments that demonstrate that engineered human brain progenitor cells, transplanted into the brains of rats and monkeys, can effectively integrate into the brain and deliver medicine where it is needed.
The Wisconsin team obtained and grew large numbers of progenitor cells from human fetal brain tissue. They then engineered the cells to produce a growth factor known as glial cell line-derived neurotrophic factor (GDNF). In some small but promising clinical trials, GDNF showed a marked ability to provide relief from the debilitating symptoms of Parkinson's. But the drug, which is expensive and hard to obtain, had to be pumped directly into the brains of Parkinson's patients for it to work, as it is unable to cross the blood-brain barrier.
In an effort to develop a less invasive strategy to effectively deliver the drug to the brain, Svendsen's team implanted the GDNF secreting cells into the brains of rats and elderly primates. The cells migrated within critical areas of the brain and produced the growth factor in quantities sufficient for improving the survival and function of the defective cells at the root of Parkinson's.........
December 20, 2005
Protein Responsible For Shaping The Nervous System
"We discovered that p63 is the major death-promoting protein for nerve cells during fetal and post-natal development," said Dr. David Kaplan, the paper's senior author, senior scientist at SickKids, professor of Molecular Genetics, Medical Genetics and Microbiology at U of T, Canada Research Chair in Cancer and Neuroscience, and co-team leader on the NeuroScience Canada Brain Repair Program grant with Dr. Freda Miller of SickKids. "Proteins such as p63 that regulate beneficial cell death processes during development may cause adverse affects later in life by making us more sensitive to injury and disease".
At birth, the nervous system has twice the number of nerve cells than needed. The body disposes of the excess cells by eliminating those that go to the wrong place or form weak or improper connections. If this process does not happen, the nervous system cannot function properly. The expression of the p63 protein guides the nervous system in disposing of the ineffective nerve cells. The protein is from the p53 family of tumour suppressor proteins that is mutated in a number of human cancers.
While p63 is involved in determining which nerve cells die, the research team also suspects that it determines whether nerve cells die when injured or in neurological and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.........
December 19, 2005
Twins Comparison Shows Genetic Factors for Dementia
The scientists suggest that these differences in thinking skills reflect a genetic risk for dementia. However, they emphasize that cognitive changes and elevated genetic risk do not always predict that twins or siblings of people with dementia will eventually develop dementia themselves.
The research, reported in the December 2005 issue of the Journal of Geriatric Psychiatry and Neurology, was led by Margaret Gatz, Ph.D., of the University of Southern California and the Karolinska Institute in Sweden. The study was funded by the National Institute on Aging (NIA), a component of the National Institutes of Health, U.S. Department of Health and Human Services, and a Zenith Award from the Alzheimer's Association. The University of Southern California Alzheimer's Disease Center is one of more than 30 Alzheimer's Disease Centers nationwide supported by the NIA.
"This research is intriguing because it associates genetic risk for dementia with twins' cognitive deficits, even in the absence of dementia," says Neil Buckholtz, Ph.D., chief of the Dementias of Aging Branch of NIA's Neuroscience and Neuropsychology of Aging Program. "The differences in cognitive deficits between identical and fraternal twins are also important, suggesting that the twins who were more similar genetically had the greater risk."
The study included 112 members of the Swedish Twin Registry who were at least 65 years old in 1998. The registry, established in 1961, includes all twins born in Sweden. Of the study participants, 23 were identical twins and 62 were fraternal twins whose co-twins had dementia but who did not have dementia themselves. A comparison group included 27 non-demented twins whose co-twins did not have dementia. The comparison group was similar to the other participants in terms of age, gender, and level of education.........
December 18, 2005
Testosterone Therapy For Alzheimer Disease
Dr. Alois Alzheimer, described Alzheimer's disease in 1906Testosterone replacement treatment may help improve the quality of life for elderly men with mild cases of Alzheimer's disease, as per a studyposted online today that will appear in the February 2006 print issue of the Archives of Neurology, one of the JAMA/Archives journals.
"There is a compelling need for therapies that prevent, defer the onset, slow the progression, or improve the symptoms of Alzheimer disease (AD)," the authors provide as background information in the article. They note that hormonal therapies have been the focus of research attention in recent years since male aging is associated with a gradual progressive decline in testosterone levels. "The gradual decline in testosterone level is associated with decreased muscle mass and strength, osteoporosis, decreased libido, mood alterations, and changes in cognition, conditions that may be reversed with testosterone replacement." The authors add that the age-related decline in testosterone is potentially relevant to AD as prior studies have found significantly lower concentrations of the hormone in middle-aged and elderly men who developed AD.
Po H. Lu, Psy.D., from the David Geffen School of Medicine, University of California, Los Angeles, and his colleagues conducted a 24-week, randomized study to evaluate the effects of testosterone treatment on cognition, neuropsychiatric symptoms, and quality of life in 16 male patients with mild AD and 22 healthy elderly men who served as controls. The study participants were randomized to receive packets of gel to apply on their skin that either contained testosterone or a placebo. Standardized tests were administered at least twice (baseline and end) during the study for the assessment of cognitive functions and quality of life.
"For the patients with AD, the testosterone-treated group had significantly greater improvements in the scores on the caregiver version of the quality-of-life scale," the scientists report. "No significant therapy group differences were detected in the cognitive scores at end of study, eventhough numerically greater improvement or less decline on measures of visuospatial functions was demonstrated with testosterone therapy compared with placebo. In the healthy control group, a nonsignificant trend toward greater improvement in self-rated quality of life was observed in the testosterone-treated group compared with placebo therapy. No difference between the therapy groups was detected in the remaining outcome measures."........
December 17, 2005
Brain Imaging to Learn if Alzheimer's Can Be Detected Earlier
MRI of BrainScientists at Emory University have received a $330,000 grant from the National Institutes of Health (NIH) and other organizations to study the use of brain imaging to identify and treat Alzheimer's disease (AD) at an earlier stage. The multi-center research trial, called the Alzheimer's Disease Neuroimaging Initiative (ADNI), will focus on brain imaging studies (MRI and PET scans) and biomarker tests (tests to detect diseases), together with measurements of memory, thinking, and daily functioning among three different groups of volunteers.
"The goal of the study is to learn how brain imaging can be used most effectively to monitor changes in the brain in Alzheimer's disease," says Allan Levey, MD, PhD, professor and chair of neurology, Emory University School of Medicine and lead investigator of the ADNI study at Emory. "Most importantly, the study will determine if brain imaging can be used to predict which healthy elderly individuals will develop mild cognitive impairment (MCI), and which individuals with MCI will go on to develop AD."
In recent years, the field of aging and dementia has moved toward trying to identify the earliest clinical signs of the process that is likely to evolve into AD. MCI has come to represent this transitional zone between the cognitive changes of normal aging and very early AD. MCI is most usually described as a subtle but measurable memory disorder. A person with MCI has memory problems greater than normally expected with aging, but does not show other symptoms of dementia, such as impaired judgment or reasoning. Researchers are still working to understand MCI and its relationship to Alzheimer's disease.
To date, this ADNI study is the most comprehensive effort to identify neuroimaging measures and biomarkers associated with cognitive and functional changes in the healthy elderly and those with both MCI and AD.........
December 17, 2005
What Can Change in the Brain?
This phenomenon is a form of neural plasticity. Chemical synapses, junctions where neurons communicate using chemical substances, have long been implicated in plasticity. Now, for the first time, Brown University researchers have demonstrated that electrical synapses are also subject to long-term changes in the brains of mammals. Their work appears in the journal Science.
"The fact that you can change the function of electrical synapses, and change them for longer than a few seconds, means that they may play a role in certain kinds of plasticity," said Barry Connors, a Brown professor of neuroscience and co-author of the paper.
"But plasticity governs a number of critical brain functions. Since electrical synapses help synchronize the activity of brain cells, these junctions probably help regulate specific brain rhythms that occur while you are awake or sleeping. So this work helps us better understand, in a basic sense, how the brain regulates behavioral states".
Carole Landisman, currently a neurobiology researcher at Harvard Medical School, is the lead author of the paper. Landisman was an investigator in Connors' lab at Brown, where the experiments were conducted.
To better understand how electrical synapses function, Landisman and Connors recorded activity from rat neurons that were connected by electrical synapses and stimulated other brain cells using brief bursts of electricity to see how the neurons would respond. They also treated neurons with two different drugs. All three techniques either activated or blocked metabotropic glutamate receptors or mGluRs, a type of neural trigger that responds to the amino acid glutamate, a transmitter molecule in the brain. The result: a long-lasting 20- to 30-percent reduction in electrical synapse strength.........
Older Blog Entries 1 2 3 4 5
Did you know?
The drug Ativan is better than Valium or Dilantin for controlling severe epileptic seizures, according to a new review of studies.Ativan, or lorazepam, and Valium, or diazepam, are both benzodiazepines, the currently preferred class of drugs for treating severe epileptic seizures. Dilantin, or phenytoin, is an anticonvulsant long used for the treatment of epileptic seizures.
Medicineworld.org: Archives of neurology news blog
The contents of this web page are protected. Legal action may follow for reproduction of materials without permission.