Scientists studying Alzheimer’s disease are increasingly finding clues that the brain begins to deteriorate years before a person shows symptoms of dementia.
The studies, published this month in the journal Lancet Neurology, found that the brains of people destined to develop Alzheimer’s clearly show changes at least 20 years before they have any cognitive impairment.
“The prevailing theory has been that development of Alzheimer’s disease begins with the progressive accumulation of amyloid in the brain,” Dr. Reiman said. “This study suggests there are changes that are occurring before amyloid deposition.”
The mutation is suspected of interfering with the brain’s ability to prevent the buildup of plaque.... The discovery, researchers say, provides clues to how and why the disease progresses. The gene, known as TREM2, is only the second found to increase Alzheimer’s risk substantially in older people. …The other gene found to raise the odds that a person will get Alzheimer’s, ApoE4, is much more common and confers about the same risk as the mutated version of TREM2
I was of the opinion that the immune system would play a fairly small role, if any, in Alzheimer’s disease,” Dr. Stefansson said. “This discovery cured me of that bias.”
“The scan was floridly positive,” said her doctor, Adam S. Fleisher, director of brain imaging at the Banner Alzheimer’s Institute in Phoenix.
The Jimenezes have struggled ever since to deal with this devastating news. They are confronting a problem of the new era of Alzheimer’s research: The ability to detect the disease has leapt far ahead of treatments. There are none that can stop or even significantly slow the inexorable progression to dementia and death.
Many insurers, including Medicare, will not yet pay for the new scans, which cost several thousand dollars. And getting one comes with serious risks. While federal law prevents insurers and employers from discriminating based on genetic tests, it does not apply to scans. People with brain plaques can be denied long-term care insurance.
Some people collect stamps, others vintage cars. As a young Ph.D. student at Cambridge University in the 1980s, Claude Wischik was on a mission to collect brains.
It wasn't easy. At the time, few organ banks kept entire brains. But Dr. Wischik, an Australian in his early 30s at the time, was attempting to answer a riddle still puzzling the scientific community: What causes Alzheimer's disease? To do that, Dr. Wischik needed to examine brain tissue from Alzheimer's patients soon after death.
He also embraced an idea that, if he is right, could ultimately spin Alzheimer's research on its heels—and raise new hopes for the roughly 36 million people world-wide afflicted with Alzheimer's or dementia.
The 63-year-old researcher believes that a protein called tau—which forms twisted fibers known as tangles inside the brain cells of Alzheimer's patients—is largely responsible for driving the disease. It is a theory that goes against much of the scientific community: For 20 years, billions of dollars of pharmaceutical investment has supported a different theory that places chief blame on a different protein, beta amyloid, which forms sticky plaques in the brains of sufferers. But a string of experimental drugs designed to attack beta amyloid have failed recently in clinical trials
A key moment came in 2008, when Dr. Wischik and Elan presented results of their studies at an Alzheimer's conference in Chicago. The Elan drug failed to improve cognition any better than a placebo pill, causing Elan shares to plummet by more than 60% over the next few days.
The TauRx results Dr. Wischik presented were more positive, though not unequivocal. The study showed that, after 50 weeks of treatment, Alzheimer's patients taking a placebo had fallen 7.8 points on a test of cognitive function, while people taking 60 mg of TauRx's drug three times a day had fallen one point—translating into an 87% reduction in the rate of decline for people taking the TauRx drug.
Molecular 'tweezers' break up toxic aggregations of proteins in mouse model
Readers recently submitted more than 100 questions about Alzheimer’s and memory loss to this week’s expert, Dr. P. Murali Doraiswamy, a psychiatry professor at Duke University Medical Center and an author of “The Alzheimer’s Action Plan.”
More than 100 other conditions, from vitamin and hormone deficiencies to rare brain disorders, can mimic Alzheimer's disease, experts say. Some are readily treatable.
Meds that Mimic Alzheimer'sPosted by Jill Fallon at November 26, 2012 6:12 PM | Permalink
Over 100 different drugs have side effects that can mimic Alzheimer's in some people. Among the most common:
Antihistimatines (Benadryl, diphenhydramine)
Sleeping pills (Ambien, Sonata)
Painkillers (Darvon, Toradol, Demerol, Naproxen, Aleve)
Anti-anxiety drugs (Valium, Librium, Halcion, Xanax)
Anti-psychotic drugs (Risperdal, Seroquel, Zyprexa)
Cholesterol drugs (Lipitor and other statins)
Older antidepressants (Elavil, Miltown, Tofranil)
Incontinence drugs (Detrol, Ditropan, Toviaz)
Acid-reflux drugs (Zantac)
Blood pressure drugs (Procardia, Adalat)
Tranquilizers (Serentil, Thorazine, Mellaril)
Heart drugs (Norpace, Lanoxin, Aldoril, Vasodilan, Cardura, Aldomet)
Stomach drugs (Bentyl, Levsin, Donnatal, Librax)
Parkinson's drugs (benztropine, trihexyphenidyl)
Source: American Geriatrics Society; Public Citizen; FDA