When high school Spanish teacher Joyce Botti started complaining about memory problems a few years ago, doctors dismissed her concerns as normal signs of aging.
But new research being presented Wednesday at an international Alzheimer's conference suggests that Botti's worries - like those of others suffering so-called "senior moments" - could be the earliest indicators of devastating brain disease.
Clemens Scherzer is caught between centuries. As a researcher-clinician, and one of three co-directors of the Harvard Biomarker Study, he spends much of the time with his eyes firmly on the future - personalised medicine for people with Parkinson's and Alzheimer's diseases. But he is also a practicing neurologist at Brigham and Women's Hospital, MA, and as such has weekly reminders of just how urgent the need for progress is.
Reisa Sperling remembers her grandfather as the robust, genial patriarch of her family. When she was young, he took her ballroom dancing and deep-sea fishing. But as he entered his seventies he became irritable and short-tempered, worried about money, and suspicious of Sperling's father and aunt, whom he accused of stealing from him. Always a dapper dresser, he began to leave his house looking dishevelled. Soon, he couldn't dress himself at all, and he eventually forgot how to use a fork and knife.
A new study has found that dementia rates among people 65 and older in England and Wales have plummeted by 25 percent over the past two decades, to 6.2 percent from 8.3 percent, the strongest evidence yet of a trend some experts had hoped would materialize.
Scientists may have uncovered a key mechanism involved in the brain degeneration seen in conditions such as Parkinson's and Alzheimer's disease.
Several neurological disorders are marked by proteins that aggregate, or accumulate in the brain. Normal proteins may become insoluble and clump together when they sporadically "misfold" and change shape. One protein, called tau, clumps into the twisted threads known as tangles that are a hallmark of Alzheimer's disease. Alpha-synuclein clumps to form the Lewy bodies associated with Parkinson's disease.
Much of what science knows about the human brain has come through deduction. If a stroke or trauma has destroyed a particular are, researchers can look at what that person can no longer do - talk, move the left pinky, do math - and infer that the affected region is linked to that behavior. In animal models, researchers often produce lesions artificially, or they inject a drug to inhibit or excite neural activity in a specific area. Yet as important as this approach has been, there are many things it can't accomplish.
In many ways, the Obama administration’s new plan to map the human brain has its origins in the work of Brenda Milner, the neuropsychologist whose detailed observations of an amnesia patient in the 1950s showed how memory is rooted in specific regions of the brain.
"Prior to Brenda Milner’s discoveries, many behaviorists and some cognitive psychologists followed the lead of Freud and Skinner in abandoning biology as a useful guide to the study of memory,” the Nobel laureate Dr. Eric Kandel wrote in his memoir, “In Search of Memory.” “Milner’s work changed all that.”
Two Harvard Stem Cell Institue (HSCI) researchers - a stem cell biologist and a practicing cardiologist at Brigham and Women's Hospital - have identified a protein in the blood of mice and humans that may prove to be the first effective treatment for the form of age-related heart failure that affects millions of Americans.
When the protein, called GDF-11, was injected into old mice, which develop thickened heart walls in a manner similar to aging humans, the hearts were reduced in size and thickness, resembling the healthy hearts of younger mice.
A large body of research has linked late-life dpression to social isolation, poorer heatlh and an increased risk of death. Now, a new study finds that depression is associated wtih subsequent vascular dementia and Alzheimer's disease, conditions poised to expand dramatically with the aging population.
Massachusetts General Hospital (MGH) investigators have determined one of the recently identified genes contributing to the risk of late-onset Alzheimer's disease regulates the clearance of the toxic amyloid beta (A-beta) protein that accumulates in the brains of patients with the disease. In their report receiving advance online publication in Neuron, the researchers describe a protective variant of the CD33 gene that promotes clearance of A-beta from the brain.