The newest FDA-approved drug for dementia is Kisunla (donanemab), approved in July 2024 for early-stage Alzheimer’s disease. It joins Leqembi (lecanemab), approved in 2023, as one of only two treatments that actually slow the progression of Alzheimer’s rather than just managing symptoms. Both drugs work by clearing toxic protein buildup in the brain, marking a genuine shift in how Alzheimer’s is treated.
How These Drugs Work
For decades, Alzheimer’s treatments could only ease symptoms like memory loss and confusion. Kisunla and Leqembi are fundamentally different: they target the underlying disease process by removing amyloid plaques, sticky protein clumps that accumulate between brain cells in people with Alzheimer’s.
Both drugs are lab-made antibodies delivered through an IV. They bind to amyloid plaques and essentially flag them for removal. The brain’s immune cells, called microglia, then engulf and break down the tagged plaques. Research published in Nature Neuroscience found that this cleanup process depends entirely on the antibody activating microglia. When researchers blocked that activation, the plaques stayed put even though the drug still attached to them. The antibodies don’t just dissolve plaques on their own; they recruit the brain’s own cleanup crew to do the heavy lifting.
How Much They Slow the Disease
In its Phase 3 trial of over 1,700 participants, Kisunla slowed cognitive and functional decline by roughly 22% to 36%, depending on the measure used and the patient population. People with lower levels of a protein called tau at the start of the trial tended to see greater benefit, with slowing closer to 35%.
Leqembi showed similar results in its pivotal trial, slowing clinical decline by about 27% over 18 months compared to placebo. In practical terms, this translates to several additional months of preserved independence and daily functioning over the course of treatment. These are not cures, and the disease continues to progress, but at a measurably slower pace.
Who Can Get These Treatments
These drugs are only for people in the earliest stages of Alzheimer’s. To qualify, you need a clinical diagnosis of either mild cognitive impairment due to Alzheimer’s or mild Alzheimer’s dementia. People with moderate or advanced Alzheimer’s are not eligible.
Beyond the clinical diagnosis, there are specific biological requirements. You need confirmed amyloid buildup in your brain, verified through either a PET scan or a spinal fluid test. Your cognitive scores must fall within a defined range, roughly corresponding to mild impairment. And a brain MRI must show fewer than four microbleeds, because existing bleeding increases the risk of side effects. In real-world clinic settings, these combined requirements narrow the eligible population considerably.
What Treatment Looks Like
Both drugs are given as IV infusions at an infusion center or clinic, but the schedules differ. Leqembi starts as a twice-monthly infusion, each lasting about an hour. After 18 months, patients can shift to once-monthly infusions or switch to a weekly self-administered injection at home.
Kisunla follows a monthly schedule from the start. The first three infusions use a lower dose, then the dose increases for subsequent sessions. One notable difference: Kisunla has a built-in stopping point. Patients get periodic PET scans to measure how much amyloid remains in their brain. Once plaque levels drop below a specific threshold, treatment stops. In the clinical trial, many patients were able to discontinue the drug within about a year. Leqembi, by contrast, is designed as an ongoing treatment without a defined endpoint.
Side Effects to Know About
The most significant risk with both drugs is a set of brain changes visible on MRI, known collectively as ARIA (amyloid-related imaging abnormalities). These come in two forms: brain swelling and small brain bleeds. In the Leqembi trial, brain swelling occurred in about 12.6% of participants. Most cases were mild and showed no symptoms, detected only on routine monitoring MRIs. Infusion-related reactions, such as chills, nausea, or flushing, affected about 26% of Leqembi patients.
Kisunla showed somewhat higher rates of brain swelling in its trial, particularly among people who carry a specific genetic variant called APOE4, which is already a known risk factor for Alzheimer’s. Both drugs require regular MRI monitoring throughout treatment, typically before dose increases and at scheduled intervals, to catch any brain changes early. In rare cases, ARIA can be serious, so this monitoring is a non-negotiable part of the treatment protocol.
Cost and Insurance Coverage
These treatments are expensive. Leqembi runs about $26,500 per year, while Kisunla costs approximately $32,000 for a 12-month course. Kisunla’s total cost may be lower in practice for patients whose amyloid clears quickly, since treatment stops once plaques are removed.
Medicare covers both drugs, but with conditions. Coverage falls under a program called Coverage with Evidence Development, meaning your prescribing doctor must submit your clinical data to a national CMS patient registry. Baseline data is submitted before your first treatment, then every six months for up to two years. This registry requirement exists because CMS wants to track how these drugs perform outside of controlled clinical trials. Private insurers vary in their coverage policies, and prior authorization is common.
What’s in the Pipeline
The current drugs focus on amyloid plaques, but Alzheimer’s involves another problematic protein called tau, which forms tangles inside brain cells. No tau-targeting therapy has been approved yet, but several are in clinical trials, including drugs called semorinemab, zagotenemab, and BIIB080. Treatments targeting brain inflammation are also under investigation. The hope is that combining amyloid-clearing drugs with therapies aimed at tau or inflammation could eventually produce larger benefits than any single approach alone.