Building on their discovery that people with Alzheimer’s have ß-amyloid deposits that appear as unusual cataracts in the lens of the eye, Lee E. Goldstein, M.D., Ph.D., of Brigham & Women's Hospital and Harvard Medical School, Boston, and colleagues have developed a new, non-invasive, laser technology that may detect Alzheimer’s at its earliest stages.
Clumps of abnormal ß-amyloid protein (known as “plaques”) accumulate outside the brain’s nerve cells in people with Alzheimer’s. As Goldstein and colleagues previously reported in the British medical journal The Lancet, these same ß-amyloid clumps also collect in the lens of the eye as unusual “supranuclear cataracts.” These Alzheimer’s cataracts are different from common, age-related cataracts. This is the first evidence to date that Alzheimer’s-related amyloid pathology may occur outside the brain.
In their most recent experiments to be reported in Madrid, the researchers used genetically engineered Alzheimer’s mice to test a new, non-invasive molecular diagnostic technology. Goldstein and his team directed a brief pulse of infrared light – barely visible to humans – into the eye of each of four non-anesthetized Alzheimer mice and four age-matched normal mice every month starting at five months of age. Analysis of how the light bounced back from the lens completely separated the two types of mice by 10 months of age, when amyloid lesions were not detectable in the brain or eye by conventional means. The scientists believe that this technology, known as quasi-elastic light scattering (QLS), may detect the very earliest stages of ß-amyloid pathology, even in eyes that are completely clear.
“Amyloid in the lens can be detected using extremely sensitive, non-invasive optical techniques. This makes the lens an ideal window for early detection and disease monitoring in Alzheimer’s,” Goldstein said.
Early identification of developing Alzheimer's might extend back by literally decades the point at which a person can be diagnosed as developing Alzheimer's. Imagine being told at, say, age 45 that 20 or 25 years from now your memory will degrade far enough that you'll have clincal Alzheimer's. I hope such people so diagnosed will react by making loud demands of their elected officials (or the dictators who rule them as the case may be) to accelerate the development of treatments. People should treat early diagnosis as a wake-up call to become politically active and fight for much larger efforts to discover the causes and cures of their diseases.
Early diagnosis will also greatly speed up research on preventive therapies, whether those therapies be drugs, diet, or other techniques. Long longitudinal studes that watch for increased risks of diseases will be replaced by shorter studies that can watch people for several years to see what factors are associated with very early stage development of Alzheimer's and other diseases of aging. Also, people so diagnosed will be able to try new therapies and scientists will be able to find out whether each therapy works before memory has degraded by a substantial amount.
The article linked to above also reports on an fMRI (functional magnetic resonance imaging) technique that finds small blood vessel ruptures may cause dementia in the elderly. Better measurement methods for this problem will lead to better ways to test therapies in shorter periods of time.
Update: Once you get the diagnosis of very early stage Alzheimer's Disease you'll of course want an immediate cure before the brain deteriorates much. Well, some Australian researchers might have the ticket. A drug called PBT2 might stop and reverse the build-up of the plaque that probably causes Alzheimer's.
Professor Ashley Bush, MD, PhD, of the Mental Health Research Institute of Victoria (Australia) and co-founding scientist of Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT) today presented data at the 10th International Conference on Alzheimer's Disease (ICAD) in Madrid demonstrating that in mouse models PBT2:
-- improved memory performance within five (5) days of oral dosing
-- rapidly reduced the levels of soluble beta-amyloid ("Abeta") in the brain, and
-- restored normal function to Abeta impaired synapses.
I'm expecting cures for Alzheimer's before cures for cancer. Preventing the build-up of a protein plaque seems a lot easier than stopping some of your own cells from dividing like mad.
The results sound promising.
In addition, Professor Bush referenced studies he and colleagues performed on 15-month old transgenic Alzheimer's mice treated with 30 mg/kg PBT2, which showed the drug reduced soluble Abeta40 and Abeta42 levels by 60 percent within 24 hours of oral PBT2 administration. Professor Bush also presented mechanistic findings showing that PBT2 blocks the copper-dependent formation of amyloid oligomers, considered by many to be the toxic chemical entity leading to brain damage in Alzheimer's disease. Professor Bush showed that, by this mechanism, PBT2 in the rodent brain blocks synaptotoxicity caused by soluble beta-amyloid oligomers and restores LTP (long-term potentiation) -- the neuronal electrical activity that underlies memory formation.
Another team has just reported preliminary results of a monoclonal antibody against Alzheimer's plaques. Drugs, vaccines, and monoclonal antibodies will all work against Alzheimer's eventually. We'd already have vaccines against Alzheimer's if the US Food and Drug Administration didn't demand excessively low levels of side effects. I'd rather run the risk of brain inflammation from a vaccine if I knew I was in the process of losing my memory and ability to think. But the FDA doesn't think we should be allowed to judge such trade-offs for ourselves.
|Share |||Randall Parker, 2006 July 23 11:24 PM Brain Alzheimers Disease|