A research team led by investigators from Massachusetts General Hospital (MGH) and Brigham and Women’s Hospital (BWH) has discovered that amyloid-beta (A-beta), the protein that forms plaques in the brains of people with Alzheimer’s disease, can also be detected in the lens of the human eye. The investigators were able to identify A-beta in lens samples from elderly individuals with and without the disorder; however, an unusual pattern of amyloid deposits was found only on the lenses of Alzheimer’s patients.
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.
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).
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.
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.