Amid a network of blood vessels and star-shaped support cells, neurons in the brain signal each other.
Image Credit: Kim Hager and Neal Prakash, University of California, Los Angeles
Alzheimer's Disease (AD) is going to become an urgent problem as last year the first of America's baby boomers began reaching their 65th birthday. The disease itself began receiving increased attention in the 1970s, although the principal contributors of the disease, high levels of amyloid and tau proteins in the brain have been known for almost 100 years.
Brain amyloid: Is it ever benign? explains that the proteins are correlated with poor mental acuity. (Memory, language, vision, and navigation.) Healthy brains don't have abnormal levels of proteins - it isn't that some people become immune to them. You can think of the tangles as simply shorting out the brain.
Researchers are developing drugs and therapies, but so far, they have not discovered a magic bullet. Untangling the Mysteries of Alzheimer's tells that scientists have identified some elementary building blocks of these proteins and tangles.
Cellular Changes in Alzheimer’s Disease explains that researchers also know that gene changes, specifically —presenilin-1 and presenilin-2 can cause early-onset AD. They have also been identified the abnormal tau protein invades cell walls and boundaries that healthy protein does not. Penetration into the dendrites disrupts chemical messaging and reception.
Brain imaging shows lifetime cognitive activity may influence Alzheimer’s disease risk explains that just as researchers have correlated the proteins with AD, they have also correlated lower levels of protein with higher levels of cognitive activity. In other words, people who stay mentally alert with games, reading, and writing, have lower amyloid and tau protein levels.
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