Major breakthrough on Alzheimer’s | The Press

A new drug, lecanemab, reduces the progression of Alzheimer’s disease by 27%, announced in the New England Journal of Medicine researchers from Yale University. The announcement dominated conversations Wednesday at a conference on Alzheimer’s in San Francisco, attended by Serge Gauthier, neurologist emeritus at McGill University. His geneticist colleague Judes Poirier believes that this is the most important advance for 20 years.

How important are the lecanemab results?

Judes Poirier (JP): The last drug for Alzheimer’s was approved 20 years ago. And this is the first time that we have seen a slowdown in progress. Current drugs, Aricept [donépézil] for example, are cognitive enhancers.

Serge Gauthier (SG): It targets an Alzheimer’s-associated protein, amyloid fibrils, found in the brain. We’ve been following the amyloid trail for a long time, this is the first time it’s worked. There is hope for other molecules that also target amyloid proteins, including a new trial with Alzheimer’s from the Montreal company Biochem. And hopefully that will convince companies to target other inflammation molecules in the brain. A Tuesday evening presentation on the impact of treatment, not included in the article, reported that the disease is significantly delayed in its progression from mild cognitive impairment to dementia. This is very significant!

Didn’t the United States approve aducanumab, a monoclonal antibody, against Alzheimer’s last year?

JP: It mysteriously passed to the FDA [Food and Drug Administration des États-Unis], even though nine of the ten scientists on the advisory board recommended otherwise. Most US insurance companies and even the Medicare program [assurance maladie publique destinée surtout aux aînés] decided not to pay. There was a decrease in amyloid protein, but no cognitive effect, unlike lecanemab.

We talked about downsides for lecanemab…

JP: There are strokes in 15% of patients, so the brain must be examined by imaging once a month to detect a possible beginning of a stroke. People who have the ApoE4 gene, which I have found to be associated with Alzheimer’s, have a higher risk of stroke. Then they could be excluded from treatment. It is also necessary to see if the slowdown in progression lasts more than 18 months.

OS: There are meetings at the congress to clarify whether the level of clinical improvement compensates for the risks of cerebral edema and cerebral hemorrhage during the first six months of treatment.

Is the cost of treatment an obstacle?

JP: In addition to the cost of lecanemab, it will be necessary to show the presence of amyloid fibrils. It can cost between $1000 and $5000. And a brain scan every month is $800 to $900. Not to mention that lecanemab is administered intravenously every two weeks. It is a challenge to install the infrastructure in Quebec with the crisis in our health system.

Aren’t there technologies detecting amyloid proteins in the blood?

JP: Yes, we do tests to show that blood detection devices are as reliable as PET scans [tomographie par émission de positons] and lumbar punctures. It could be used to detect asymptomatic patients and prevent Alzheimer’s from appearing.

Could lecanemab be approved quickly?

OS: Within a year in Canada, in my opinion. A group in Quebec is already working on the organization of intravenous administration. We think it could be home nurses. It was done for a drug pilot project for young people.

Are there other similar drugs in preparation?

JP: Results on another molecule targeting amyloid proteins are expected within the next month or two. But we had negative results for a similar molecule at the beginning of November.

OS: I think in my lifetime I will see a significant improvement in the prognosis of Alzheimer’s. An editorial published Wednesday in the Journal of Prevention of Alzheimer’s Disease said that with lecanemab, a turning point has been reached.