My late father had a longtime friend, a retired kosher butcher, who lived down the hall in their South Jersey apartment building. Past 90, Manny was older and frailer than my father; he leaned on a cane and could barely see well enough to recognize faces. But every morning, and again in late afternoon, he walked through my dad’s unlocked front door to be sure he was all right and to kibitz a bit.
The Alzheimer's Drug Discovery Foundation (ADDF) announced today the launch of Cognitive Vitality, a new online resource developed to provide a comprehensive and credible overview and analysis of the science for specific strategies to prevent Alzheimer's and related dementias.
What non-amyloid targets should be pursued for Alzheimer's disease therapies? We put the question to three well-known researchers in the field: Bradley Hyman, MD, PhD, of Massachusetts General Hospital in Boston; John Trojanowski, MD, PhD, of the University of Pennsylvania in Philadelphia; and Richard J. Caselli, MD, of the Mayo Clinic in Scottsdale, Ariz.
Their answers ranged from tau protein pathologies to apolipoprotein E to general neuroprotection.
Doctors commonly use magnetic resonance imaging (MRI) to diagnose tumors, damage from stroke, and many other medical conditions. Neuroscientists also rely on it as a research tool for identifying parts of the brain that carry out different cognitive functions.
Alzheimer's disease isn't what it used to be. After 30 years of having doctors diagnose the disease by symptoms alone, researchers and advocacy groups are calling for new diagnostic criteria that recognize changes in the brain as well as changes in behavior.
The goal is to eventually allow doctors to diagnose "preclinical" Alzheimer's in patients who do not have problems with memory or thinking, but who do have an abnormal brain scan or some other sign that the disease may be developing.
Why do neurodegenerative diseases such as Alzheimer’s affect only the elderly? Why do some people live to be over 100 with intact cognitive function while others develop dementia decades earlier?
More than a century of research into the causes of dementia has focused on the clumps and tangles of abnormal proteins that appear in the brains of people with neurodegenerative diseases. However, scientists know that at least one piece of the puzzle has been missing because some people with these abnormal protein clumps show few or no signs of cognitive decline.
A Boston scientist poised to launch a pioneering Alzheimer’s prevention study was awarded an $8 million grant Thursday to expand the research and further explore potential causes of cognitive decline in the mind-robbing disease.
Dr. Reisa Sperling, a neurologist at Harvard Medical School and an Alzheimer’s specialist at Brigham and Women’s Hospital, received the Alzheimer’s Association grant, the largest such research award the group has ever given, the association said.
Harvard stem cell scientists have successfully converted skins cells from patients with early onset Alzheimer’s into the types of neurons that are affected by the disease, making it possible for the first time to study this leading form of dementia in living human cells. This may also make it possible to develop therapies more quickly and accurately than before.