Scientists are peeking inside living brains to watch for the first time as a toxic duo of plaques and tangles interact to drive Alzheimer's disease -- and those tangles may predict early symptoms, a finding with implications for better treatments. It's not clear exactly what causes Alzheimer's. Its best-known hallmark is the sticky amyloid that builds into plaques coating patients' brains, but people can harbor a lot of that gunk before losing memories. Now new PET scans show those plaques' co-conspirator -- the tangle-causing protein tau -- is a better marker of patients' cognitive decline and the beginning of symptoms than amyloid alone. That's especially true when tau spreads to a particular brain region important for memory, researchers reported Wednesday in the journal Science Translational Medicine.
Long before symptoms like memory loss even emerge, the underlying pathology of Alzheimer's disease, such as an accumulation of amyloid protein plaques, is well underway in the brain. A longtime goal of the field has been to understand where it starts so that future interventions could begin there. A new study by MIT neuroscientists at The Picower Institute for Learning and Memory could help those efforts by pinpointing the regions with the earliest emergence of amyloid in the brain of a prominent mouse model of the disease. Notably, the study also shows that the degree of amyloid accumulation in one of those same regions of the human brain correlates strongly with the progression of the disease. "Alzheimer's is a neurodegenerative disease, so in the end you can see a lot of neuron loss," says Wen-Chin "Brian" Huang, co-lead author of the study and a postdoc in the lab of co-senior author Li-Huei Tsai, Picower Professor of Neuroscience and director of the Picower Institute.
Researchers may have discovered the'ground zero' of Alzheimer's disease, paving the way to treatment that could halt condition in its tracks. A team of scientists at the University of North Carolina's Medical School conducted a series of experiments to look at different factors driving the disease in order to try and pinpoint a way to stop it in its tracks. Alzheimer's disease causes abnormal deposits of amyloid beta protein and tau protein in the brain, as well as swarms of activated immune cells. The team of researchers used different experiments to look at how the proteins and activated immune cells attack the brain and cause Alzheimer's-related symptoms. The drug, called tubastatin A, is currently undergoing late stage clinical trials at a number of hospitals around the United States.
Another one bites the dust. Pharmaceutical giant Merck has halted a trial of a promising Alzheimer's drug, verubecestat, after it was determined that there was virtually no chance of it working. This comes just two months after the failure of another Alzheimer's drug, solanezumab. Both drugs target beta amyloid plaque, the sticky gunk that accumulates in the brains of people with the disease. These failures have revived doubts over the long-held theory that beta amyloid is crucial in causing the disease.
Certain antibodies may be able to remove Alzheimer's plaques from the brain, according to new research carried about in mice. As much as 20 years before the symptoms of Alzheimer's set in, people with the disease begin to develop amyloid beta plaques that build up in the brain and, scientists believe, interfere with neural signals to cause cognitive and memory losses. But researchers at Washington University School of Medicine have developed an antibody that can remove the proteins these plaques are made of altogether, according to their new research. Several recent clinical trials have tried to use antibodies to target the plaques, but none have gotten past these trial phases, and many treatments have come with unsustainable side effects. The new approach may offer a way around these side effects and stop Alzheimer's plaques before its heart-breaking symptoms begin, the researchers hope.