Lecanemab: Alzheimer’s cure or not?
Tokyo pharmaceutical company, Eisai and biotechnology firm, Biogen recently develop a breakthrough for Alzheimer drug candidate using monoclonal antibody that slowed rate of cognitive decline. Scientists are very curious about it but some are hesitant about it, why is that?
Lecanemab treatment is indeed a breakthrough!
Lecanemab has been claimed to slow the rate of cognitive decline by 27%. But hey, only 27%? Doesn’t that seem to be too low? Then why it’s called a breakthrough? It’s because this is the most encouraging result to date. Yes, previous treatments’ attempt at targeting amyloid doesn’t have good result in the clinical trial.
Lecanemab is a monoclonal antibody. It works by clearing clumps of amyloid within our brains. Once patients show mild cognitive impairment, usually they have around 6 years of living independently. If we slowed cognitive decline by 27% that will give an extra 19 months for patients of living independently.
Lecanemab works by clearing amyloid. However, amyloid has not been confirmed to be the cause of dementia in Alzheimer’s case. Hence, lecanemab is dealing with one of the associated proteins causing dementia but not the source of the problem itself.
and that’s why some scientists argue that
The target should have been tau protein instead of amyloid
But why? It’s because cognitive decline correlates strongly* with tau protein instead of amyloid. Research using a mouse model shows that amyloid accumulation did not cause nerve cell death. Recently, by using more advanced imaging scientists were able to observe amyloid accumulation in the brain. Brain scans of patients show that there are some Alzheimer patients with low amyloid accumulation and also there are healthy people with some amyloid deposits in the brain.
*Takes note that the keyword is correlate strongly and not exact cause or something similar.
So why are companies developing treatments targeting amyloid instead of tau? Are they going to make some expensive treatment with low efficiency to make a huge profit? I don’t think so.
I think it’s because the hypothesis that stated amyloid as the cause of Alzheimer’s had been around since 1991, so it has been around for at least 20 to 30 years meanwhile tau protein correlation with neuron degradation is found in 2017.
Because of the time difference, drugs targeting tau protein is still being developed by scientist meanwhile drugs targeting amyloid is already developed and just need more refinement to increase their efficiency. Also, several drug trials with tau protein as a target have failed in the clinical trial. Currently, there are 11 clinical trials of tau protein-targeted immunotherapies with most of them at phase 1 or 2.
However, scientist still needs to research more about tau protein, drug, side effect, etc. Meaning that it will take some more time for the development of effective therapies against tau protein.
Combined efforts of drug targeting both amyloid and Tau for more effective treatment of Alzheimer’s
As you can see, we need to develop drugs targeting tau protein. However, that doesn’t mean drug-targeting amyloid is useless. Lecanemab can still slow the rate of cognitive decline by 27%. But how? As we discussed before in the mice model nerve cell death was not observed but in another research that also uses the mice model, it has been suggested that amyloid causes synaptic impairment.
So in the near future when effective treatment targeting tau protein has been developed, we can combine drugsthat targets amyloid and tau protein together to slow neuron degradation and hopefully it will be able to do it.
