Where Next For Alzheimer's Treatment?

So if the Tau-ists are right, the door to an inflammatory-model treatment for Alzheimer's based on an anti-inflammatory diet and anti-inflammatory drugs aimed at reducing amyloid plaque as an inflammation by product slams shut. 

But do the Tau-ists open another door even as they close what once appeared to be a promising line of enquiry into Alzheimer's?

Maybe. There's a trial at Harvard under way right now that's screening patients for Tau as well as beta-amyloid, the specific amyloid responsible for plaques in the brain. And the transfer of attention from amyloid to Tau can't come quickly enough in the drugs industry. Pharmaceutical companies have developed drugs that target amyloid plaques and reduce the amount of beta-amyloid in the brain, but none of them has been able to show that it can affect the course of Alzheimer's. So shifting focus to Tau might mean we're at least working on the right problem.

And the work has already begun. As long ago as July of 2014, scientists at a conference in Copenhagen presented their plans for Tau-based therapies. Methods that are being explored include active vaccines, an antibody, an inhibitor that stops the enzyme that removes sugar molecules from Tau and an anti-aggregating compound. One therapy works by injecting antibodies that attack and clear Tau from the brain, while another the enzyme-based treatment is expected to be effective because Tau steadily sheds sugar as people age. Preventing Tau from shedding sugar is expected to restore Tau to the function it would have in a younger person and prevent the neuron damage that leads to Alzheimer's.

Some of these, including one of the vaccines, have already completed rounds of testing in mice and in almost every case human trials are under way. In some cases, these are working with groups of people who are suffering from diseases like progressive supranuclear palsy, which is a rare and fast-acting disease caused by Tau pathologies.

There's also hope that treatments that help Alzheimer's patients might be effective for a wide range of illnesses. If everything about the amyloid hypothesis is correct except whcih brain protein is to blame, then the raft of expectations that attached itself to amyloid therapies doesn't have to be abandoned. It can attach itse;f almost unchanged to Tau therapies. If Tau treatments work against Alzheimer's they might also be effective against Parkinson's or even CJD.

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