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.
A new drug treatment stops the progression of Alzheimer's disease in monkey brains, scientists report. The drugs – called CpG oligodeoxynucleotides (CpG ODN) – prompt immune defence cells to swallow misshapen proteins – amyloid beta plaques and tau tangles. The build-up of these misshapen proteins is known to kill nearby brain cells, causing the debilitating disease, which is the most common type of dementia in the UK. In lab trials, elderly monkeys had up to 59 per cent fewer amyloid beta plaque deposits in their brains after CpG ODN treatment compared with untreated animals. Alzheimer's disease is thought to be caused by the abnormal build-up of proteins in and around brain cells.
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.
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.
An eye test could spot Alzheimer's disease two decades before symptoms emerge, a new study claims. Comparing their results to brain scans, the eye test was just as successful at spotting those with twice the amount of plaque build-up in their brains. Experts say the finding is one of the biggest breakthroughs in Alzheimer's research to date, offering the first sign of a cost-effective and non-invasive test. 'The findings suggest that the retina may serve as a reliable source for Alzheimer's disease diagnosis,' said the study's senior lead author, Dr Maya Koronyo-Hamaoui, a neurosurgeon at Cedars-Sinai. An eye test developed by researchers in Los Angeles managed to spot Alzheimer's-related plaque build-up in the brain before symptoms had fully emerged (file image) Alzheimer's disease is a progressive, degenerative disease of the brain.