Alzheimer's disease
Researchers at NYU School of Medicine have found that immunization prolongs the incubation period for prion diseases such as Creutzfeldt-Jakob disease and may have therapeutic value for other neurodegenerative illness such as Alzheimer's disease. Prion disease is a fatal brain disease manifested through failure of muscle control and dementia. Forms of this disease have been discovered in deer and elk (chronic wasting disease), in cows (bovine spongiform encephalopathy ? BSE ? or "mad cow disease") and in sheep (scrapie strain).
Researchers have found evidence that non-steroidal anti-inflammatory drugs (NSAIDs) including ibuprofen, aspirin, and naproxen, may exert a protective effect against the risk of Alzheimer's disease. Results of their epidemiological, multiple-study analysis of nearly 16,000 patients are being presented at the American Academy of Neurology Annual Meeting in Honolulu, March 29-April 5, 2003.
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.
A new Mayo Clinic study shows that the fears of many related to living into one's 90s and beyond -- getting lost in your own neighborhood; losing the ability to take care of financial affairs; having a driver's license revoked; ending up in a nursing home -- are in many cases unfounded. This research, to be published in the Feb. 11 issue of Neurology, demonstrates that for many age 90 and above, memory can be strikingly sharp even up to one century of age.
Greater insight into human brain disease may emerge from studies of a new genetic mutation that causes adult fruit flies to develop symptoms akin to Alzheimer's disease. "This is the first fruit fly mutant to show some of the outward, physical manifestations common to certain major human neurodegenerative diseases," said principal investigator Michael McKeown, a biology professor at Brown University. A research team found the mutation in a gene they named "blue cheese."
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
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.
U.S. government scientists have demonstrated that a miniature positron emission tomography (PET) scanner, known as microPET, and the chemical markers used in traditional PET scanning are sensitive enough to pick up subtle differences in neurochemistry between known genetic variants of mice. This "proof-of-principle" experiment "opens up a whole new, non-invasive way to study and follow transgenic or genetically engineered strains of mice that serve as animal models for human neurological diseases, such as Parkinson's and Alzheimer's disease or psychiatric diseases such as substance abuse, depression, and anxiety disorders," said Panayotis (Peter) Thanos, lead author of the study.
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.
The hunt to find a gene that causes a disease typically costs hundreds of thousands of dollars and requires years of research - and it still may fail to turn up the sought-after culprit, driving the research back to square one. The result is that while the genes involved in a few inherited diseases such as cystic fibrosis have been identified, many have not. Now, two scientists say they may have found a way to make the search more economical and speed it up. In an article to appear online in the Proceedings of the National Academy of Sciences next week, scientists from the University of Florida and Purdue University report merging two established genetic-screening techniques to create one that's better. The new technique narrows the pool of "candidate" genes in a study from thousands of possibilities to fewer than 100 - perhaps as few as 20.
Researchers say they've developed a new test for prions that improves the accuracy and speed with which the malformed and infectious proteins can be detected. Prions cause neurodegenerative diseases in sheep, deer and elk, plus Mad Cow disease in cattle and Creutzfeldt-Jakob in humans.
