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…
A medication used to treat the symptoms of mild-to-moderate Alzheimer disease may actually do more – it may be able to delay progression of the disorder, according to a study conducted at the Indiana University School of Medicine. The study, which appears in the June issue of Archives of Neurology, enabled researchers to evaluate a change in cognition observed in patients who prematurely discontinued treatment with placebo or Exelon ? (rivastigmine tartrate), a medication prescribed for many patients.
A new imaging technique that could lead to optical biopsies without removal of tissue is being reported by biophysical scientists at Cornell and Harvard universities. The advance in biomedical imaging enables noninvasive microscopy scans through the surface of intact organs or body systems. Demonstrations of the new technique are producing images of diseased tissue at the cellular level with unprecedented detail.
Hopes that naproxen, a nonsteroidal anti-inflammatory drug (NSAID), or rofecoxib, a COX-2 inhibitor, could slow the progression of Alzheimer’s disease (AD) have been dashed as researchers at Georgetown University Medical Center report in the June 4 Journal of the American Medical Association that neither drug slows the cognitive deterioration that is the hallmark of AD. In addition, more adverse effects were reported in patients taking either drug as compared to the placebo group.
A team of researchers from Imperial College London, the Charing Cross Hospital and University College London have identified a protein which could be used to protect against neuro-degenerative conditions such as Alzheimer’s, Parkinson’s, Huntington’s, motor neurone diseases and the damage caused by strokes.
Researchers at Emory University and Argonne National Laboratory have discovered a new method to manipulate the self-assembly and formation of amyloid fibrils, a major component of brain plaques associated with Alzheimer’s disease, thereby opening new avenues for examination of their formation and for the construction of robust nanotubes that have potential applications in research, industry and medicine.
Why do serious diseases such as cancer, Alzheimer’s and Huntington’s mainly hit us in middle age or later? The links between aging and age-related diseases have proved elusive. In studies of the powerfully informative roundworm, C. elegans, UCSF scientists have discovered that a class of molecules found in the worms and in people can both prolong life in the worm and prevent the harmful accumulation of abnormal proteins that cause a debilitating Huntington’s-like disease. The finding appears to be the first evidence in an animal of a link between aging and age-related disease.
Scientists at the Center for the Study of Macular Degeneration at the Neuroscience Research Institute of the University of California, Santa Barbara have found a link between the brain plaques that form in Alzheimer?s disease and the deposits in the retina that are associated with age-related macular degeneration (AMD). AMD is a disease that leads to loss of central vision and affects 5 to 10 percent of the population over age 60.
A new MR imaging technique used to study white matter in the brain has found something intriguing–the brains of Alzheimer’s patients show some of the same signs as the immature brains of children. Diffusion tensor MR imaging examinations were performed on 60 normal persons, ranging in age from infancy to late adulthood, says Jeffrey Lassig, MD, of the University of Michigan, and lead author of the study. The part of the brain that connects the two halves of the brain was studied. When the brain is immature the water molecules in the white matter of the brain move (diffuse) more freely. As the brain ages, the water molecules seem more constrained, he says.
Researchers have discovered an important similarity in the causes of cell degeneration and death in diseases such as Alzheimer’s, Parkinson’s, Huntington’s, type II diabetes and CJD, suggesting that a single therapy could combat these different ailments.
Researchers have discovered an important similarity in the causes of cell degeneration and death in diseases such as Alzheimer’s, Parkinson’s, Huntington’s, type II diabetes and CJD, suggesting that a single therapy could combat these different ailments. University of California at Irvine molecular biologists Charles Glabe and Rakez Kayed found that small toxic molecules believed to trigger cell damage in these diseases have a similar structure. The study, which appears in the April 18, 2003 issue of Science, implies that these molecules, called toxic soluble oligomers, share parallel functions, which makes them suitable targets for new drugs or vaccines that could halt progression of many degenerative diseases.
Opening a new front in the battle against Alzheimer’s disease, scientists at the University of Pennsylvania have found that a protein long associated with the disease inflicts grave damage in a previously unimagined way: It seals off mitochondria in affected neurons, resulting in an “energy crisis” and buildup of toxins that causes cells to die. This pathway, the first specific biochemical explanation for pathologies associated with Alzheimer’s, is detailed in the April 14 issue of the Journal of Cell Biology.