t’s easy to think that the mysteries of Alzheimer’s disease will be revealed in the high-tech hallways of US medical centers and research institutes. But new discoveries are coming from far-off places like Medellín, Colombia, which may be ground zero for finding the genetic basis of this dreaded neurodegenerative disease that strips people of memories and destroys personalities.
Thousands of gene candidates in the human genome have the potential to play a role in the onset and progression of Alzheimer’s disease. But you are just one scientist. How can you even start such an enormous task? This quest - one scientist analyzing thousands of gene candidates - can seem overwhelming.
Harvard Medical School researchers at Boston Children’s Hospital explain in a new paper how brain connections, or synapses, are lost early in Alzheimer’s disease. They also show that the process starts before telltale plaques accumulate in the brain.
Their work, published online March 31 in Science, suggests new therapeutic targets to preserve cognitive function early in Alzheimer’s disease.
More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons.
“It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville.
Even the simplest networks of neurons in the brain are composed of millions of connections. Examining these vast networks is critical to understanding how the brain works, and now, an international team of researchers, led by Wei-Chung Allen Lee, instructor in neurobiology at Harvard Medical School, R. Clay Reid of the Allen Institute for Brain Science in Seattle and Vincent Bonin of Neuro-Electronics Research Flanders (NERF), has published the largest network to date of connections between neurons in the visual cortex.
In the early stages of Alzheimer’s disease, patients are often unable to remember recent experiences. However, a new study from MIT suggests that those memories are still stored in the brain — they just can’t be easily accessed.
The MIT neuroscientists report in Nature that mice in the early stages of Alzheimer’s can form new memories just as well as normal mice but cannot recall them a few days later.
The National Institute on Aging (NIA) and the National Institute of Neurological Disorders and Stroke (NINDS), both part of the National Institutes of Health (NIH), have launched the Molecular Mechanisms of the Vascular Etiology of Alzheimer’s Disease (M²OVE-AD) Consortium to better understand how the body’s vascular system, its network of large and small blood vessels, contributes to Alzheimer’s disease.
Toxic buildup of a protein in the brain's language centers may help drive a rare form of dementia that causes people to lose their ability to use language, a new study finds.
Researchers at Northwestern University in Chicago used high-tech imaging to track the buildup of amyloid protein in the brains of people with the language-loss dementia, called primary progressive aphasia (PPA).
They compared those findings to amyloid buildup in the brains of people with memory loss related to Alzheimer's disease.
“The number of Americans with Alzheimer’s disease and other dementias will grow each year as the size and proportion of the U.S. population age 65 and older continue to increase. The number will escalate rapidly in coming years as the baby boom generation ages.” 2015 Alzheimer’s disease Facts and Figures
Marty and Matt Reiswig, two brothers in Denver, knew that Alzheimer’s disease ran in their family, but neither of them understood why. Then a cousin, Gary Reiswig, whom they barely knew, wrote a book about their family, “The Thousand Mile Stare.”
When the brothers read it, they realized what they were facing.