Arnaud Pontin (Image : AI / Gay Globe)
A new drug for Alzheimer’s disease, donanemab, has just been approved by Health Canada and could also potentially help slow certain neurological symptoms associated with HIV.
Donanemab is a new medication intended for certain people with early-stage Alzheimer’s disease. Marketed under the name Kisunla, it was approved in the United States by the FDA in July 2024. It is primarily intended for people with mild cognitive impairment or mild dementia associated with Alzheimer’s disease.
Unlike medications that mainly seek to temporarily improve certain symptoms, donanemab targets one of the biological mechanisms characteristic of the disease: the accumulation of beta-amyloid proteins in the brain.
How does donanemab work?
To simplify, we can imagine that certain proteins gradually accumulate in the brain and form deposits called amyloid plaques. These deposits are associated with processes that contribute to the deterioration of nerve cells observed in Alzheimer’s disease.
Donanemab is a monoclonal antibody designed to recognize a particular form of beta-amyloid found in these plaques. It therefore helps the immune system eliminate these deposits. Studies have indeed shown a significant reduction in the amount of amyloid plaques in treated patients.
The goal is therefore not to make memory problems disappear instantly, but rather to slow the progression of the disease.
This is probably the most important element to understand.
Donanemab does not cure Alzheimer’s disease and does not restore normal memory. Clinical trials have shown that, on average, treated patients experienced slower cognitive and functional decline than those who received a placebo.
In the study that led to its approval, involving 1,736 people, the drug produced a statistically significant reduction in the decline observed after 76 weeks. In other words, the disease continues to progress, but it may progress more slowly in some people.
Donanemab is intended for the early stages of the disease. This is important because brain damage associated with Alzheimer’s begins to develop long before dementia becomes severe.
Researchers therefore believe that it is more beneficial to intervene when damage to the brain is still relatively limited. Treatment also requires confirmation of the presence of amyloid pathology before it can begin.
Donanemab is not, however, a risk-free medication. It can cause abnormalities visible on brain imaging known as ARIA, which include swelling or small areas of bleeding in the brain. These complications are often asymptomatic, but they can sometimes be serious.
How does donanemab work?
There is an interesting scientific hypothesis concerning donanemab and certain neurological complications of HIV, but it is important to be very precise: donanemab is currently not a treatment for HIV, and it has not been demonstrated to improve HIV-related cognitive disorders.
In some people living with HIV, even when the virus is perfectly controlled with antiretroviral therapy, chronic inflammation of the nervous system may persist and cognitive disorders may develop under the term HAND (HIV-associated neurocognitive disorders). These can include problems with memory, attention, concentration, or the speed at which information is processed.
The potential connection lies in the brain and the beta-amyloid protein. Donanemab is designed to eliminate the beta-amyloid deposits characteristic of Alzheimer’s disease.
However, scientific research shows that HIV and the chronic inflammation associated with HIV can disrupt beta-amyloid metabolism. Proteins produced by HIV could, in particular, promote its production or reduce its elimination.
This raises an interesting question: could a drug capable of eliminating beta-amyloid potentially have a role in some people living with HIV who develop neurocognitive disorders?
But there is an important problem: studies conducted in people with HAND do not show that amyloid accumulation is systematically comparable to that observed in Alzheimer’s disease. One study involving people with controlled HIV, for example, found that, at the group level, amyloid accumulation was similar to that seen in older people without cognitive impairment, and significantly lower than that observed in groups with mild cognitive impairment or Alzheimer’s disease.
So, for now…
Donanemab could be interesting for research into HIV-associated cognitive disorders, but it should absolutely not be described as an existing treatment for HIV or HAND.
The scientific interest would instead be to determine whether a subgroup of people living with HIV actually has Alzheimer’s-type amyloid pathology. In these individuals, an anti-amyloid treatment could potentially be studied.
Donanemab does not treat HIV, but its mechanism could become a research avenue for certain neurological disorders observed in people living with HIV, particularly when biological characteristics of Alzheimer’s disease are present.
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