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Tuesday 19th June 2018

Protein linked to Alzheimer's

21st September 2010

In the brains of people who suffer from Alzheimer's disease, beta-amyloid is just one factor that causes mental degeneration, according to a recent US study.


Beta-amyloid is a sticky substance which ends up coating the brain in Alzheimer's patients.

Drug companies have spent money developing anti-amyloid compounds only to find that such drugs do more harm to the brain than good.

Recently, scientists have discovered that a type of brain protein called 'tau protein' often appears misfolded in Alzheimer's patients.

Tau protein tends to clog brain cells and rapidly accelerates the development of Alzheimer's disease in people who have a certain genetic mutation.

Study author Alison Goate, a senior researcher at Washington University in St Louis, said that figuring out how to lower people's tau levels might slow dementia.

Currently, the medications that are available for Alzheimer's ease people's symptoms, but do nothing to halt or even slow the progress of brain degeneration.

In addition to pointing the way to possible treatments, the recent study may also end up helping families to know how much time they have until a person with Alzheimer's cannot function independently at all.

When tau protein begins to clog the brain, its form changes slightly, and it becomes phosphorylated tau (ptau).

Ptau gets released into people's spinal fluid when the cells harbouring it die.

Using measurements of spinal fluid, the researchers were able to identify one gene that seemed to contribute to the brain getting clogged.

While identifying the role of tau protein in the brain, and the genes associated with its production, was an important step, it is still too early for scientists to use genetic tests to look for at-risk patients.

Goate said it was likely that more than one genetic marker for tau protein susceptibility would be discovered by scientists.

She said that people with low levels of tau protein tended to get Alzheimer's later on than people with a lot of the substance.

Some drug companies are already at work on drugs that aim to limit tau production in the brain, including a Singapore company which has begun advanced research trials on an anti-tau drug called LMTX.

John Trojanowski, a researcher at the University of Pennsylvania, whose organisation collaborates with AstraZeneca to identify anti-tau compounds, said that he and his colleagues had believed for some time that Alzheimer's disease could not be pinned down to any one treatment method.

Paul Aisen, a dementia specialist at the University of California in San Diego, said that the new research would not make research on amyloid plaque less important.

He said that both amyloid plaque and tau protein were important, and that both substances represented areas where drugs could be developed.

The problem is that autopsies have found amyloid plaque in elderly people whose memories still worked well, implying that drugs which only focus on amyloid plaque will not do Alzheimer's patients any good.

Some companies are beginning to test vaccine-like therapies for tau protein in mice.

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