Posted by WBHI on Mar 8, 2013 in Think Ahead
by Jason Gate for Bloomberg:
Abnormal deposits in the brain thought to trigger Alzheimer’s disease can be detected decades before the memory-robbing illness ensues, a finding that will help guide future treatments, researchers in Australia said.
Doctors at Melbourne’s Austin Hospital followed 200 seniors, including people with Alzheimer’s disease and mild cognitive impairment, for more than three years to chart any decline in cognition and brain size against the deposition of abnormal protein in their brains. They found it takes about 20 years for the deposits, known as amyloid beta, to lead to dementia.
Posted by WBHI on Feb 13, 2013 in Sooner Than You Think
by Science Daily:
A study combining genetic data with brain imaging, designed to identify genes associated with the amyloid plaque deposits found in Alzheimer’s disease patients, has not only identified the APOE gene — long associated with development of Alzheimer’s — but has uncovered an association with a second gene, called BCHE.
A national research team, led by scientists at the Indiana University School of Medicine, reported the results of the study in an article inMolecular Psychiatry posted online February 19. The study is believed to be the first genome-wide association study of plaque deposits using a specialized PET scan tracer that binds to amyloid.
The research also is believed to be the first to implicate variations in the BCHE gene in plaque deposits visualized in living individuals who have been diagnosed with Alzheimer’s disease or are at-risk for developing the disease. The enzyme coded by the BCHE gene has previously been studied in post-mortem brain tissue and is known to be found in plaques.
Posted by WBHI on Dec 18, 2012 in Wishful Thinking
by Tess Stynes for 4-Traders:
Merck & Co. reached a collaboration, license and supply agreement with General Electric Co.’s health-care business for use of a GE Healthcare investigational imaging agent to support the pharmaceutical company’s lead drug candidate to treat Alzheimer’s disease.
Merck’s investigational Alzheimer’s treatment–called MK-8931–targets a substance in the brain called amyloid. Scientists have hypothesized that the buildup of amyloid in the brain plays a role in Alzheimer’s disease. A number of major pharmaceutical companies have been looking for a treatment to stop the progression of the disease, which impairs memory and cognitive skills in the elderly.
by Jason Tin for The Courier-Mail:
Dementia patients are slowly rediscovering their former selves by cuddling robotic baby seals, dinosaurs and cats as part of an ambitious research project.
Masked by an adorable and convincing exterior, the Japanese-manufactured hi-tech robots can follow voices, respond to changes in pressure and touch, learn their names, respond to light, snuggle up to those cuddling them and gently fall asleep when left alone.
The models are so realistic many of the elderly test subjects seem unable to distinguish them from real animals.
Led by Griffith Health Institute’s Professor Wendy Moyle, the study aims to determine if the robots can help patients learn to communicate and express joy again.
Posted by WBHI on Jun 12, 2012 in Sooner Than You Think
by Charles Bankhead for MedPage Today:
Brain imaging with a beta amyloid-specific tracer identified patients who had a high risk of rapid progression from mild cognitive impairment to Alzheimer’s disease, an Australian study showed.
Three-fourths of patients with high uptake of 18F-florbetaben (18FBB) progressed to Alzheimer’s disease within 24 months. In contrast, half of patients with hippocampal atrophy met diagnostic criteria for Alzheimer’s disease within 2 years.
The results suggest that PET imaging with18FBB could offer the earliest test yet developed for diagnosis of Alzheimer’s disease, according to a study reported at the Society of Nuclear Medicine meeting in Miami Beach, Fla.
Posted by WBHI on May 23, 2012 in Think About It
by David Krotz for Berkeley Lab:
For the past five years, volunteers from the City of Berkeley and surrounding areas have come to Lawrence Berkeley National Laboratory to participate in an ongoing study that’s changing what scientists know about Alzheimer’s disease.
The volunteers, most over the age of 70, undergo what can best be described as a brain checkup. They’re asked to solve puzzles and memorize lists of words. Magnetic resonance imaging (MRI) scans image the structure of their brains in exquisite detail. Functional MRI scans allow scientists to watch portions of their brains light up as they form memories. And Positron emission tomography (PET) scans measure any accumulation of beta-amyloid, a destructive protein that’s a hallmark of Alzheimer’s.
The goal of the Berkeley Aging Cohort Study is to reveal how our brains change as we age. The scientists also compare their findings with brain scans of Alzheimer’s patients. They’ve noticed something odd—and perhaps a little hopeful. Some volunteers have the same level of beta-amyloid deposition as an Azheimer’s patient. Yet they show no signs of the disease.
Why is this? How can two people, the same age and with the same signs of the disease, take such different paths?
Posted by WBHI on Apr 25, 2012 in Sooner Than You Think
by Pauline Anderson for Medscape News
Misdiagnosis of Alzheimer’s disease (AD) based on positron emission tomography (PET) scan readings appears to be a troubling problem that could get worse as more amyloid-specific tracers become available.
A new study found that almost two thirds of patients were misdiagnosed or had inconclusive data on the basis of interpretation of their PET scan in a community setting.
“We concluded that since this is such a large percentage of people who are misdiagnosed based upon their PET scans that we should caution clinicians to weigh the risks versus the benefits before ordering PET scans,” said Sheena M. Shipley, BS, Departments of Neurology and Psychiatry, University of Colorado School of Medicine, Denver. She presented the data here at the American Academy of Neurology’s 64th Annual Meeting.
The US Food and Drug Administration (FDA) approved fluorodeoxyglucose (FDG)-PET in 2004 for the diagnostic evaluation of dementia. Previous studies had shown that this test can assist in the differential diagnosis of frontotemporal dementia and AD.
The research to date has shown varying diagnostic accuracy for PET, said Shipley.
Posted by WBHI on Apr 16, 2012 in Sooner Than You Think
by Melissa Healy for Los Angeles Times
No one wants to hear that he or she has Alzheimer’s disease. But if the beta-amyloid plaques that are the disorder’s key physical hallmark could be detected before memory loss and cognitive troubles were evident to all, would you want to know? And since no treatment currently works to stem the inexorable progress ofAlzheimer’s, who would pay for a costly test to detect it early — and why?
Those questions are no longer hypothetical. Last week, the FDA approved an agent called Florbetapir F 18 injection (to be marketed as Amyvid), which will allow physicians using a positron emissions tomography (PET) scan to detect the presence and extent of amyloid plaques in patients concerned about declining mental function.
And on Monday, the American Academy of Neurology released a new study showing that an agent called florbetaben also allowed detection of amyloid plaques when used with a PET scan. The florbetaben is to be presented at the academy’s “Emerging Science” program next week in New Orleans. Both Florbetapir F 18 and florbetaben help diagnose Alzheimer’s by sticking to beta amyloid clumps and emitting radioactivity, which can then be picked up by a PET scan.
Posted by WBHI on Apr 15, 2012 in Wishful Thinking
by Charlene Laino for WebMD
An experimental drug called florbetaben may help doctors diagnose Alzheimer’s disease earlier in some people with memory problems.
Florbetaben is one of several new radioactive agents that tag the amyloid plaque that builds up in the brains of people with Alzheimer’s disease. Others include Amyvid, approved last week by the Food and Drug Administration.
After florbetaben is injected into the brain, the plaques that are a hallmark of Alzheimer’s disease — light up when a patient has a brain imaging scan called positron emission tomography (PET), says Marwan Sabbagh, MD, director of Banner Sun Health Research Institute in Sun City, Ariz.
In late-stage testing, Sabbagh and colleagues compared PET scans using florbetaben taken from 31 people in the months before they died to brain tissue taken at autopsy. The presence of amyloid plaque at autopsy is currently the only way to confirm a diagnosis of Alzheimer’s.
The scans correctly identified 100% of people who had plaque at autopsy, but one person who tested positive for plaque did not end up having any — a small dent in the test’s accuracy.
Posted by WBHI on Mar 16, 2012 in Think About It
by Becky McCall for Medscape
Beta-amyloid burden present in the brains of healthy controls before the appearance of symptoms indicates potential for future cognitive impairment and Alzheimer’s disease (AD), according to research presented here at the Alzheimer’s Disease International (ADI) 27th International Conference.
David Ames, MD, professor of ageing and health, and director, National Ageing Research Institute at the University of Melbourne, Australia, leads the Australian Imaging Biomarkers and Lifestyle (AIBL) flagship study of aging, which looks at amyloid protein brain imaging, blood biomarkers, and lifestyle factors in the detection and prevention of early AD.
According to Dr. Ames, the 3-year follow-up data are particularly exciting because they support the association between amyloid protein build-up in the brain and future cognitive impairment. “We need to follow people up for longer, but we do see a correlation between 3-year decline on memory tests and the amount of amyloid in the brain at baseline in apparently healthy older people,” he said.
The study shows that if an individual meets clinical criteria for mild cognitive impairment (MCI) and has amyloid protein in the brain, within 3 years there is a greater than 50% risk that person will have AD, whereas that risk is less than 10% for those with MCI who are free of amyloid at baseline.