Science is a slogan. Not a series of “Eureka!” moments.
That’s why I hate the word “breakthrough” when it comes to research findings.
but in this case New drug for Alzheimer’s The word makes sense.
Not because lecanemab is a cure for a disease that is destroying hundreds of thousands of lives in the UK at any one time. It is not.
It’s a breakthrough because it’s the first positive sign that our painstaking, decades-long effort to find a cure for Alzheimer’s is about to pay off.
It all comes down to a rogue protein called amyloid that builds up in the brains of Alzheimer’s patients. This protein acts like molecular junk that clogs up and eventually kills brain cells.
The genetic basis of this process was first shown 30 years ago by Professor John Hardy at University College London.
It has led to a surge in research and investment by pharmaceutical companies into drugs that can clear up amyloid and remove it from brain cells.
Over the years, many treatments that worked in the laboratory entered clinical trials. Some have been shown to be very effective at removing amyloid from people’s brains. But none had any measurable effect on Alzheimer’s symptoms.
As the failures ensued, some researchers began to wonder whether the “amyloid hypothesis” for the cause of Alzheimer’s disease was correct. Major pharmaceutical companies investing in amyloid-targeting drugs are starting to get disappointed and scale back their investments.
Urgent need to detect disease before symptoms appear
Likonumab Looks like it’s going to change all that. Not only does it show that the amyloid hypothesis may be correct — it could also explain why previous drugs have not been successful.
Clinical trials of lecanemab have shown that it clears amyloid from the human brain faster than previous drugs. Given that clinical trials typically run for only a year or two, some experts believe the fact that lecanemab works faster than other drugs is why they were able to detect a small but measurable slowdown in Alzheimer’s symptoms in people taking the drug.
This has two important implications. First, it means that if people take the drug for longer, its beneficial effects may increase over time.
But it also illustrates the importance of giving people drugs like lecanemab before amyloid causes widespread damage. While trials showed that Alzheimer’s disease progression slowed slightly in people taking the drug, their symptoms continued to worsen. The theory is that the amyloid they live with has already done the damage, and drugs may not help reverse it.
That means there is an urgent need for better tests to detect Alzheimer’s before symptoms start to appear, so that lecanemab, and the drugs that are sure to come, can be tested earlier.
If this breakthrough revives efforts to find more amyloid-fighting drugs, and at the same time develop better tests, a true cure for this dreaded disease may not be far away.