Alzheimer's
The supplement dehydroepiandrosterone, or DHEA, which has been touted by some as an anti-aging hormone and a treatment for diseases such as cancer, AIDS, diabetes and Alzheimer's disease, showed no effect for Alzheimer's disease patients who took the supplement for six months, according to a study published in the April 8 issue of Neurology, the scientific journal of the American Academy of Neurology. DHEA is a hormone produced naturally in the adrenal glands. The body then converts it into the hormones estrogen and testosterone. DHEA as a supplement is made from plant chemicals.
A drug that quashes the activity of a key brain chemical is the first effective treatment for patients in the later stages of Alzheimer's disease, according to the results of a large multi-center clinical study published in the April 3 issue of the New England Journal of Medicine. The drug, memantine, slows the mental and physical deterioration of patients with moderate to severe Alzheimer's disease, according to Barry Reisberg, M.D., Professor of Psychiatry at NYU School of Medicine, who led the study. "These patients seem to be declining much less, about half as much as ordinarily expected, over a six-month period," says Dr. Reisberg. "This medication will slow down the otherwise inexorable progress of this disease, and it is remarkably free of side effects. These are very impressive results. It looks like this drug really will have an impact on this disease," he says.
A molecule that naturally degrades a protein linked to Alzheimer's disease appears to reduce the levels of that protein by nearly 50 percent when delivered by gene therapy, researchers at the Salk Institute and UC San Diego have found in collaboration with researchers at the University of Kentucky. The findings appear in the March 15 issue of the Journal of Neuroscience.
In a breakthrough study, scientists have found that common painkillers such as ibuprofen and naproxen may actually dissolve the brain lesions -- or amyloid plaques -- that are one of the definitive hallmarks of Alzheimer's disease. The findings are reported in the March 31 issue of Neuroscience. Principal investigator Jorge R. Barrio, professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA, has used FDDNP, a new chemical marker developed in his laboratory at UCLA, to visually zero in on the brain lesions present in Alzheimer's disease. He discovered that common over-the-counter pain medications -- known as non-steroidal anti-inflammatory drugs -- bind to amyloid plaques, and may help dissolve existing plaques and prevent the formation of new ones.
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.
Some of the most important compounds are the shortest lived -- transient molecules that exist for only thousandths of a second or less during chemical reactions. Characterization of such "reaction intermediates" can play a key role in understanding the mechanisms by which molecules change, shedding light on processes ranging from basic chemical reactions to complex diseases such as Alzheimer's. Yet by their very nature, reaction intermediates exist for brief periods too short to be seen by most sensors.
Based on recent findings of 12 new potential sites for Alzheimer's genes, a leading researcher estimates that within 50 years, patients will be routinely screened for Alzheimer's Disease and receive prescription drugs tailored to their genetic risk. Speaking at the American Association for the Advancement of Science (AAAS) Annual Meeting in Denver today, Rudolph E. Tanzi, director of the Genetics and Aging Research Unit at the Massachusetts General Hospital, said that his research and that of other geneticists offers hope that physicians eventually will be able to predict and prevent the disease that poses a serious threat to the minds of millions of aging baby boomers.
UCLA and University of Queensland (Australia) neuroscientists using a powerful new imaging analysis technique have created the first three-dimensional video maps showing how Alzheimer's disease systematically engulfs the brains of living patients. The findings appear in the Feb. 1 edition of the peer-reviewed Journal of Neuroscience. The dramatic time-lapse videos show the sequential destruction of brain areas that control memory function, then emotion and inhibition, and finally sensation. They also show how the disease spares small brain regions that control vision and other functions that remain intact in Alzheimer's patients
A group of Canadian researchers has found the most direct evidence to date that people with early-stage Alzheimer Disease can engage additional areas in the brain to perform successfully on memory tests. Alzheimer's is a progressive, degenerative disease that affects an individual's ability to think, remember, understand and make decisions. People with early-stage Alzheimer's begin to experience problems with their episodic and semantic memory. Semantic refers to the accumulation of general world knowledge gained over a lifetime (for example, names of countries, famous people, major historical events). Episodic refers to events that one experiences throughout his/her life (for example, having visited the dentist yesterday, or graduating from college back in 1950).
They are proteins that cut other proteins, enabling a wide range of essential functions such as wound healing, blood clotting and formation of muscle and nerve cells.
But serine proteases also can cut a path of destruction, contributing to the plaques involved in heart disease and Alzheimer's and to extensive birth defects as well when something goes awry. Understanding this sort of physiological crescendo called a protease cascade is a goal of Dr. Ellen K. LeMosy, developmental biologist at the Medical College of Georgia.
Agents that alter blood levels of beta-amyloid protein in mouse models of Alzheimer's disease represent a potential approach to treating the illness in humans that may be safer than the vaccine method of therapy, researchers report in a new study. Beta-amyloid protein is a component of the amyloid plaques that accumulate in the brains of people with Alzheimer?'s disease. Beta-amyloid is viewed by many researchers and clinicians as the underlying cause of the degeneration and dementia that characterize the illness. Alzheimer's disease is a progressive, degenerative brain disease and the most common form of dementia. There is no cure.
Scientists have averted the onset of neurodegenerative disease in fruit flies by administering medication to flies genetically predisposed to a disorder akin to Parkinson's disease. The result suggests a new approach to the treatment of human disorders including Parkinson's and Alzheimer's diseases. Parkinson's disease is the second most common human neurodegenerative disorder, characterized by tremors, postural rigidity and progressive deterioration of dopaminergic neurons in specific areas of the brain. Despite the evolutionary gulf separating humans and fruit flies, neurotoxicity unfolds in a similar manner in both species.
Researchers have discovered a way to refine an experimental Alzheimer's vaccine, a finding that could pave the way for new treatment and prevention of the debilitating disease that affects people's ability to think and recall information. Alzheimer's occurs when toxic biochemical compounds known as amyloid-beta peptides accumulate in the brain, forming plaque deposits and injuring nerve cells, which eventually causes dementia. In 2000, researchers at the Centre for Research in Neurodegenerative Diseases published a paper showing how the amyloid-beta peptide vaccine blocked the production of the plaques and reversed learning impairment. The vaccine stimulates the body's immune system into forming antibodies against the plaques in the brain, but it also caused inflamation. This new research claims to have found a way to better isolate the active epitope detected by antibodies. After testing a more refined, targeted amyloid-beta vaccine on mice, the scientists found that the antibodies generated by the vaccine cleared away the plaques -- improving cognitive function in the mice and leaving no evidence of brain inflammation.
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.
Federal researchers say they've developed several drug candidates that show promise in protecting the brain against damage from stroke, with the potential to fight chronic neurodegenerative conditions like Parkinson's and Alzheimer's disease as well.. The drugs, called p53 inhibitors, attack a key protein involved in nerve cell death and represent a new strategy for preserving brain function following sudden injury or chronic disease.
