Every 66 seconds, someone in the U.S develops Alzheimer’s Disease (AD), and the Centers for Disease Control and Prevention estimate that each year about 93,000 people die from the condition. Despite these startling statistics, we still know very little about the disease. However, a new study from Australia has “completely changed our understanding” of how AD affects the brain, shedding light onto the nerve cell processes that lead to the condition, and perhaps even opening the door for new treatment options.

The formation of protein plaques and tangles on the brain is the hallmark of AD. Researchers have long believed that the plaque-forming protein, amyloid-beta, caused a modification called phosphorylation to the tau protein. The phosphorylation of tau protein was thought to result in cell death which ultimately led to Alzheimer's disease. However, the new study suggests that phosphorylation of tau protein has a protective, not destructive, effect on the brain cells. Eventually this defense is worn down, ultimately leading to AD.

"Amyloid-beta induces toxicity in the neurons but the first step in tau phosphorylation is actually to decrease this toxicity," explained lead study Professor Lars Ittner in a recent statement. "This is a completely new mindset; that the reason tau becomes modified is actually to protect from damage."

The team was able to find this potentially groundbreaking discovery on AD’s pathology by studying the disease's progression in mice and human brain tissue.

Alzheimer’s disease is the most common form of dementia, and is characterized by memory loss and thinking and behavioral problems. According to the Alzheimer’s Association, scientists can see abnormal buildups of protein fragments between nerve cells called plaques. When these nerve cells die they cause “tangles.” While researchers can see the result of AD, they are not completely sure of what causes these deformations. The new theory on the roots cause of AD could have far-reaching uses.

The research is still in its early years, but the team eventually plans to work on treatments based on their research.

“If we can stimulate that activity, we may be able to delay or even halt the progression of Alzheimer's disease," added Ittner.

Source: Ittner A, Wern Chua S, Bertz J, et al. Site-specific phosphorylation of tau inhibits amyloid-β toxicity in Alzheimer’s mice. Science . 2016

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