Alzheimer’s disease destroys brain cells and their connections (called synapses), causing memory loss and other cognitive problems that disrupt work, hobbies and daily life. Symptoms can be alleviated, in part, by the drug memantine (marketed in the…
People with high levels of iron in their diet are more likely to develop Parkinson’s disease, according to a study in the June 10 issue of Neurology. People with both high levels of iron and manganese were nearly two times more likely to develop the disease than those with the lowest levels of the minerals in their diets. The study compared 250 people who were newly diagnosed with Parkinson’s to 388 people without the disease. Interviews were conducted to determine how often participants ate certain foods during their adult life.
By pumping a potent growth factor directly into the human brain, an international team of scientists and surgeons has demonstrated significant remediation of the debilitating symptoms of patients with Parkinson’s disease.
Blocking or eliminating a specific potassium channel in a small group of brain cells may improve or prevent the symptoms of Parkinson’s disease, a debilitating and progressive neurodegenerative disease that afflicts over 1 million people in the United States. In Parkinson’s disease, neurons that release dopamine die. The loss of dopamine causes an array of debilitating symptoms that include resting tremor, muscle rigidity and slowed movement. Although the cause of the disease remains uncertain, James Surmeier and colleagues at Northwestern University have discovered a way of potentially lessening the symptoms and progression of the disease. The investigators describe their findings in the March issue of Nature Neuroscience.<
Scientists have discovered how estrogen initiates physical changes in rodent brain cells that lead to increased learning and memory — a finding, the researchers contend, that illustrates the likely value of the hormone to enhance brain functioning in women. Their study, published in the March 15 issue of The Journal of Neuroscience, describes for the first time a chain of molecular events that is activated in the brain’s primary memory center, called the hippocampus, when estrogen bathes nerve cells.
Blocking or eliminating a specific potassium channel in a small group of brain cells may improve or prevent the symptoms of Parkinson’s disease, a debilitating and progressive neurodegenerative disease that afflicts over 1 million people in the United States. In Parkinson’s disease, neurons that release dopamine die. The loss of dopamine causes an array of debilitating symptoms that include resting tremor, muscle rigidity and slowed movement.
A new study from Columbia University College of Physicians and Surgeons (P&S) and Stanford University suggests that the malfunctioning of brain cells called astrocytes may be behind the accumulation of amyloid protein in the brains of patients with Alzheimer’s disease. Alzheimer’s disease, most researchers believe, is caused when small peptides called beta-amyloid accumulate in the brain. Everyone makes these peptides at all times during their life, but in people with Alzheimer’s, either too much is made or too little is degraded or both.
Studying mice, scientists have successfully prevented a molecular event in brain cells that they’ve found is required for storing spatial memories. Unlike regular mice, the engineered rodents quickly forgot where to find a resting place in a pool of water, the researchers report in the March 7 issue of the journal Cell. The experiments are believed to be the first to prove that subtly altering the chemistry of a certain protein can profoundly affect a brain cell’s ability to respond to external stimulation, a process called neuronal plasticity, long thought to underlie learning and memory.
Medical advice rarely supports a high-fat diet, but a team of UC Irvine researchers has found that such a diet protects newborn brain cells from damage caused by prolonged seizures. New findings from a study on infant rats suggest that the high-fat diet of newborns, and the related increased production of a specific protein, protects their brain cells from damage that otherwise may accompany prolonged seizures. The finding may lead to new strategies to prevent brain injury in adults.
Researchers have published new evidence showing that cells from the bone marrow might help repair or maintain cells in other tissues. In a paper in this week’s online edition of the Proceedings of the National Academy of Sciences, the researchers describe finding chromosomes from a bone marrow transplant in the brain cells of transplant recipients. When people receive a bone marrow transplant after high-dose chemotherapy, some of the transplanted cells regenerate the blood-making cells that were destroyed. In past experiments in mice, scientists found that cells from the transplant could also relocate to tissues throughout the body rather than being restricted to the bone marrow and blood.
A Mayo Clinic investigation of Interleukin-6, a hormone inside cells often considered a “bad actor” of the immune system because of its association with inflammation injuries and malignant diseases, shows that it also plays a therapeutic role in mice: it protects brain cells. Interleukin-6 — called IL-6 for short by researchers — may, in fact, be a “white knight” for mouse brain cells, or neurons, as brain cells also are called. These results, while early, may be promising for humans as well. The Mayo Clinic investigation is described in the Jan. 15 Journal of Neuroscience.
New research results strongly suggest that cocaine bites the hand that feeds it, in essence, by harming or even killing the very brain cells that trigger the “high” that cocaine users feel. This most comprehensive description yet of cocaine-induced damage to key cells in the human brain’s dopamine “pleasure center” may help explain many aspects of cocaine addiction, and perhaps aid the development of anti-addiction drugs. It also could help scientists understand other disorders involving the same brain cells, including depression.
Trimming the waistline may not be the only reason to cut calories after the New Year: Doing so also may protect the brain from aging. In the first study to look specifically at the effects of life-long calorie-restricted diets on brain cells, University of Florida researchers determined certain proteins linked to cell death that naturally increase with age were significantly reduced in the brains of rats whose calories were limited. More important, they found the levels of a beneficial protein known to provide potent protection against neuron death were twice as high in older rats whose calories were restricted by 40 percent.
A compound that enables squirrels to hibernate may one day help minimize brain damage that results from stroke. In an animal model for stroke, delta opioid peptide reduced by as much as 75 percent the damage to the brain’s striatum, the deeper region of the brain and a major target for strokes, according to researchers. In fact, evidence suggests that the compound, which puts cells in a temporary state of suspended animation, may help protect brain cells from the ravages of Parkinson’s disease as well.
Biologists have shown for the first time in the laboratory that they can convert some adult human neural stem cells to brain cells that can produce dopamine, the brain chemical missing in Parkinson’s disease. If the researchers can better understand the process and harness this ability, the work may someday lead to new strategies in treating neurodegenerative diseases such as Parkinson’s.
A seemingly mild “insult” to the brain could sensitize neurons to attack by immune system proteins that are otherwise protective, researchers have found. The finding could explain why sufferers of Alzheimer’s and other neurodegenerative diseases significantly worsen following such insults. The scientists believe that drugs to selectively inhibit the immune proteins could reduce the rate of neural damage in a wide range of neurodegenerative diseases. Such drugs could also protect other organs against damage from autoimmune diseases such as lupus and rheumatoid arthritis, in which the immune system attacks body tissues.
Brain cell membranes have established “doorways” that accept or reject molecules trying to pass into the cell, researchers have founbd. The discovery fundamentally changes how researchers think about the behavior of neurons. It had been long believed that surface molecules such as receptors are enveloped right where they rest in the fatty membrane, to be drawn into the cell’s interior.
Researchers have discovered a gene mutation that causes a condition apparently identical to Huntington’s Disease, helping explain why some people with the disorder do not have a separate mutation found in most cases. The finding may help reveal why some diseases, like Huntington’s, Alzheimer’s and Parkinson’s, destroy some brain cells while sparing others. “For all practical purposes this is Huntington’s Disease, yet it’s caused by a different mutation on a completely different chromosome,” said Russell L. Margolis, M.D., associate professor of Psychiatry at Hopkins and director of the Johns Hopkins Laboratory of Genetic Neurobiology. “This is a rare version of an already rare disorder, but the mutation that causes it may not only help us better understand Huntington’s Disease, but could boost our understanding of many other neurodegenerative disorders.”
