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.
Using a little creativity and a lot of new technology, Mass General researchers have created a new generation of brain mapping images that promises to open the door to understanding and treating brain disorders.
Neurologist Bruce Miller calls tau—a floppy, free-form protein—“the holy grail of dementia.” That designation may come as a surprise to anyone who has even a passing interest in the science of end-of-life brain diseases. A different protein, amyloid-beta (Aß), has become famous as the culprit responsible for the so-called senile plaques that gum up the brains of people with Alzheimer’s disease.
As if people reaching their middle years didn't have enough to keep them awake at night—mortgage payments, job demands, the angst of teenage children - a study by French and British researchers last year concluded that our brains start to decline around age 45, smack in the prime of middle age.
Known for decades as patient H.M., Henry Molaison was familiar, indeed dear, to neuroscientists. In 1953, epilepsy surgery to remove a tiny part of his brain left him forever unable to acquire new facts and store them.
In China, there are only about 300 qualified physicians to treat more than 9 million dementia sufferers. The shortage is overwhelming families and threatening resources from an already stretched welfare system as the country ages.