There are currently 143 drugs in 172 clinical trials for the treatment of Alzheimer’s. Of these, 119 drugs have been described as disease modifying. These are designed to alter the underlying biology of the disease
Alzheimer’s causes memory loss.
The Conversation: Around 55 million people around the world have some kind of dementia is, in which Alzheimer’s Most common. Unfortunately, there is no cure for this memory-depriving disease. But a lot of people’s hopes were pinned on an experimental drug named Gentanerumab. A recent press release by the drug maker Roche did not bring good news. The injected drug had no significant effect on the symptoms of Alzheimer’s or on a protein called amyloid responsible for the disease. .
Gentanerumab is an antibody that attaches itself to amyloid. On the other hand, amyloid is a sticky protein that keeps accumulating in the brains of people suffering from Alzheimer’s. As soon as this antibody binds to Amyloid, the brain’s natural defense system is triggered, which removes Amyloid. Smaller trials of gantenorumab supported this view. Because it had a positive effect on the symptoms of the disease and reduced Amyloid clusters.
But its trials on a large scale failed to replicate the initial success, which once again raises questions about targeting Amyloid. The causes of Alzheimer’s disease are not yet known, but the most popular explanation is the so-called “Amyloid cascade hypothesis”.
Changes seen in the brain of people with Alzheimer’s disease
This hypothesis, proposed 30 years ago, describes a series of events that lead to Alzheimer’s disease. The scientists’ hypothesis is based on changes observed in the brains of people with Alzheimer’s disease, as well as genetic evidence from families whose successive generations developed Alzheimer’s.
The changes he noticed in the brain were the accumulation of clumps of amyloid proteins called plaques, and accumulations of tau proteins, called tangles. The hypothesis holds that amyloid plaque formation is the initial process of the disease. Plaques then attach to other brain cells and blood vessels, disrupting their normal function and eventually killing neurons (brain cells).
Scientists have refined this hypothesis over the past 30 years, as new information was discovered on the biological processes underlying Alzheimer’s disease. That’s why drug manufacturers have a special focus in targeting Amyloid.
The disappointing results for gantanerumab also add to a long line of reported failures of drugs targeting amyloid clumps. The repeated failures (14 in total) have fueled the debate whether targeting amyloid is the right approach.
What causes Alzheimer’s disease
Proponents of the amyloid cascade hypothesis may argue that the failure of experimental drugs may reflect deficiencies in trial designs, for example in how the drugs are administered or the stage of disease at which the drugs are given.
While detractors may argue that other changes in the brain such as tau tangles are more closely related to the symptoms of dementia and should be targeted.
The debate is not over and will not be resolved by the positive and negative test results that come next. This is meaningless and diverts attention from the question of what causes Alzheimer’s disease. Amyloid is clearly associated with the development of Alzheimer’s disease as are many other proteins. But does the focus on amyloid divert attention from other potential targets? Other hypotheses exist, but have they been adequately tested? We can guess the answer to these questions from the list of Alzheimer’s drugs being developed.
There are currently 143 drugs in 172 clinical trials for the treatment of Alzheimer’s. Of these, 119 drugs have been described as disease modifying. These are designed to change the underlying biology of the disease – not just treat the symptoms. Of the 119 disease-modifying drugs, only 20 have amyloid as a primary target.
Most researchers agree that there is no single cause of Alzheimer’s disease. It has been proven that the symptoms and changes in the brain are unique to each person – but with some common features. Targeting a single feature is unlikely to make a significant difference in Alzheimer’s disease, but the depth and diversification of existing therapies suggests we are on the right track in understanding and treating Alzheimer’s.
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Source: www.tv9hindi.com”