Stunning Alzheimer’s discovery could lead to treatment

Stunning Alzheimer’s discovery could lead to treatment

It's a big discovery that could have huge ramifications for the treatment of Alzheimer's disease.

A new study offers tremendous hope for sufferers of Alzheimer’s disease, and could eventually lead to new treatments.

Researchers say they were able to use a newly developed mouse model that mimics the development of Alzheimer’s in humans, revealing that a “one-two punch” of biological “insults” must happen for it to result in dementia, according to a Johns Hopkins Medicine statement.

Scientists have long known that Alzheimer’s disease is associated with abnormal clumps of protein called tau within brain nerve cells, as well as by deposits of protein called beta-amyloid in brain tissue. But scientists have been unable to determine the relationship and timing in the two clumping processes, as one occurs outside of cells while the other occurs inside.

This new study indicates that accumulating beta-amyloids isn’t enough to trigger the conversion of tau, and in fact it may actually set off a chain of chemical signaling events that result in the conversion of tau into a clumping state — meaning scientists may have just found a process that can be disrupted.

In humans, it can take up to 15 years or more for this chain reaction to complete, which makes it difficult to study in mice. So researchers genetically engineering a mouse model that promoted the clumping of tau.

“For the first time, we think we understand that the accumulation of amyloid plaque alone can damage the brain, but that’s actually not sufficient to drive the loss of nerve cells or behavioral and cognitive changes,” Philip C. Wong, Ph.D., professor of pathology at the Johns Hopkins University School of Medicine, said in the statement. “What appears to be needed is a second insult — the conversion of tau — as well.”

It’s possible the research may explain why some drugs designed to attack the disease after the conversion of tau haven’t worked as well as had been hoped.

“The timing may be off,” Wong said. “If you were to intervene in the time period before the conversion of tau, you might have a good chance of ameliorating the deficits, brain cell loss and ensuing consequence of the disease.”



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