Lecanemab and Donanemab: what the new Alzheimer's drugs can and cannot do
If someone in your family has been diagnosed with Alzheimer's, you've probably seen the headlines about two new drugs. Lecanemab and donanemab. Breakthrough, they said. The first treatment to go after the disease itself.
That part is true. These are the first drugs that clear a harmful protein out of the brain and slow the illness down, rather than just taking the edge off the symptoms. After thirty years of failed attempts, that's a real scientific first.
But three things sit underneath those headlines. These drugs don't stop Alzheimer's, and they don't give back memory that's already gone. They aren't routinely available on the National Health Service (NHS). And they're licensed only for people at the earliest stage of the disease who also meet a set of safety criteria, which rules out a great many people with a diagnosis.
One bit of vocabulary before we start, because it comes up throughout. When scientists call a result "statistically significant", they're saying the numbers they got would be an unlikely thing to see if the drug did nothing at all, and that is the whole of what it means. It doesn't tell you how big the benefit is, or whether anyone would notice it in daily life. Those are two different questions.
What the drugs do
Alzheimer's involves several things going wrong at once. The one that's dominated research for thirty years is a protein fragment called amyloid-beta (Kepp et al., 2023).
A healthy brain makes amyloid-beta and clears it away again, as part of its normal housekeeping. In Alzheimer's, the clearing-away stops working properly. The fragments clump into sticky deposits called plaques, and those build up between the nerve cells for years, sometimes decades, before anyone notices a symptom (Kepp et al., 2023). Picture a drain silting up over years. Water still goes in, less comes out, and the blockage keeps growing.
Plaques probably aren't the whole story, and researchers are still working on other proteins. But amyloid changes can be detected years before any symptoms appear. Lecanemab (sold as Leqembi) and donanemab (Kisunla) are monoclonal antibodies. An antibody is a protein your immune system uses to latch on to one specific target, rather like a key cut for a single lock. These two are manufactured antibodies, designed to find amyloid-beta and stick to it. Once they've stuck, they flag the deposit for removal by the brain's own clean-up cells (van Dyck et al., 2023; Sims et al., 2023). Lecanemab targets the small, soluble clumps that form before they harden into plaques; donanemab targets a modified form found inside plaques that have already hardened.
What makes these two different from everything before them is straightforward. Earlier drugs had cleared amyloid out of the brain over and over again without helping anyone think or function any better. These are the first to clear amyloid and slow the decline, in large, properly run trials (van Dyck et al., 2023; Sims et al., 2023). That link between the target and the result is what makes this a milestone.
How much benefit was seen?
There were two big trials. CLARITY AD tested lecanemab in 1,795 people with early Alzheimer's over eighteen months (van Dyck et al., 2023). TRAILBLAZER-ALZ 2 tested donanemab in a similar group over the same stretch of time (Sims et al., 2023).
Both tracked a scale called the Clinical Dementia Rating Sum of Boxes, or CDR-SB. It was the main measure in the lecanemab trial; the donanemab trial used a different main measure and tracked the CDR-SB alongside it, which at least gives us one common yardstick. The two drugs have never been tested head to head (Sims et al., 2023).
The CDR-SB scores six parts of ordinary life. Memory. Knowing where you are and what day it is. Judgement and problem-solving. Getting out and about. Hobbies and life at home. Washing and dressing. Each one is scored nought to three, so the total runs from nought, meaning no problems at all, up to eighteen, meaning very severe impairment (van Dyck et al., 2023). Someone at the early stage these trials studied might be somewhere around two to five.
In the lecanemab trial, people on the dummy infusion got worse by 1.66 points over eighteen months. People on the drug got worse by 1.21 points. Neither group held steady. The gap between them was 0.45 points (van Dyck et al., 2023). That was the average difference on the trial's main clinical measure over eighteen months.
What does a gap that size mean for a person?
The clearest way to answer that is in time rather than points. When the National Institute for Health and Care Excellence (NICE) assessed both drugs, it judged the benefit to be a delay in the disease's progression of roughly four to six months (National Institute for Health and Care Excellence, 2025). The disease is delayed, not halted and not reversed, and those few months are ground that would otherwise have been lost.
That estimate describes a trial population, not a person. It isn't something measured individually, and it doesn't predict how long anyone will keep any particular ability. Nobody can tell you that your mother will still be doing the crossword next autumn.
The donanemab trial did something slightly different. Its headline results come from a group it called the low/medium tau population, picked out by levels of a second protein called tau, where a lower level means the disease is at an earlier stage. In that group, people on placebo got worse by 1.88 points and people on the drug by 1.20 points, a gap of 0.67 points. Across everyone in the trial, including people further along, the gap was 0.70 points, slightly wider in raw terms but a smaller share of a steeper decline (Sims et al., 2023).
You'll also see all this written up as percentages. A 27% slowing for lecanemab. 36% for donanemab in the low/medium tau group, or around 29% across the whole trial (van Dyck et al., 2023; Sims et al., 2023). Those figures are accurate, and they're the ones that tend to end up in headlines. But they describe the gap as a slice of the decline, not as a slice of what the person can still do. The percentage tells you how the two groups compared with each other. It doesn't tell you how much ability anyone kept.
Both trials also counted how many people crossed over into the next stage of the disease during the study, and fewer did on the drugs than on placebo (van Dyck et al., 2023; Sims et al., 2023). That is easier to picture than a shift in test scores, though it isn't stronger evidence, just a different way of reporting the same result.
Beyond eighteen months ...
Longer-term follow-up is available. Extension studies of both drugs report benefits continuing past eighteen months (Zimmer et al., 2025; van Dyck et al., 2025). These are harder to interpret than the original randomised comparisons.
People first assigned to placebo were later given the active drug, so the studies stopped comparing treatment against no treatment. Some analyses instead compared outcomes against separate observational groups of people who had never been in the trial. In the donanemab extension, which stayed blinded, participants whose scans showed the amyloid had cleared were switched to placebo infusions. Who entered the extensions, who left them, and how the comparison groups differed all add uncertainty.
Other work has questioned the picture of increasing benefit, using published summary results and computer simulations rather than the original patient records. It does not establish that the drugs cause faster decline (Dwivedi et al., 2026).
Longer-term findings exist, then, and the size and durability of the benefit remain uncertain.
Risks and treatment burden
Both drugs carry a real risk of something called ARIA, which stands for amyloid-related imaging abnormality. It means changes that turn up on a magnetic resonance imaging (MRI) scan while the amyloid is being cleared out. It takes two forms, swelling and tiny bleeds.
Most of these changes are spotted on a scan rather than felt by the patient, and you need to hold that distinction when you read the numbers.
In the lecanemab trial, swelling showed up on the scans of 12.6% of people taking the drug, against 1.7% on placebo. Of those taking the drug, 2.8% had symptoms from that swelling (van Dyck et al., 2023). When symptoms do come, they're usually headaches, dizziness, confusion, or trouble with vision. Small bleeds were also more common on both drugs than on placebo. Donanemab's rates were higher, with swelling on the scans of 24% of people taking it and 6.1% getting symptoms from it (Sims et al., 2023). The donanemab trial recorded a small number of deaths where ARIA may have played a part (Sims et al., 2023).
The risk climbs steeply in people carrying a gene variant called apolipoprotein E4, or APOE4, which happens to be the strongest common genetic risk factor for Alzheimer's in the first place. Everyone considered for either drug is tested for it beforehand (Eisai, 2026; Eli Lilly, 2026).
Then there is what treatment actually involves, which weighs on most families as heavily as the trial figures.
Neither drug is a tablet. Both are given by drip at a hospital or clinic. Lecanemab is given every two weeks to begin with, and after eighteen months either carries on fortnightly or moves to four-weekly maintenance (Eisai, 2026). Donanemab is given every four weeks, at a lower dose for the first three infusions and a higher one after that, and stops once scans confirm the amyloid has cleared, or at eighteen months at the latest (Eli Lilly, 2026). Lecanemab has no fixed end point, though it is stopped if the disease progresses to moderate Alzheimer's.
Scans punctuate the whole course. Both drugs need a recent MRI before the first infusion and further scans at set points during treatment, because the swelling has to be looked for whether or not the patient feels anything (Eisai, 2026; Eli Lilly, 2026). If a scan picks something up, treatment may be paused or stopped. Reactions to the infusion itself are common rather than rare: in the lecanemab trial, 26.4% of people had one (van Dyck et al., 2023).
For a family, that adds up to hospital trips every two or four weeks over many months, somebody free to go along, repeated scans, and a course that might be interrupted. It belongs in the decision alongside the four to six months.
Who is eligible?
The rules are narrow. If you're reading this hoping these drugs might be an option for someone you love, this is the section to read closely.
Both trials only took people at the earliest stages, meaning either mild cognitive impairment, where the memory problems are noticeable but daily life still works, or mild dementia. Amyloid had to be confirmed first, by a positron emission tomography (PET) brain scan or by testing the fluid around the spine (van Dyck et al., 2023; Sims et al., 2023). Nobody with moderate or severe Alzheimer's was included, and there's no evidence the drugs help at that stage.
Two different sets of rules get muddled together constantly, so it helps to take them separately.
The trials themselves turned away people with recent strokes, certain heart conditions and various other problems. They did, however, include people carrying two copies of APOE4, and the higher swelling rates in that group are part of what the trials reported.
The UK licences are tighter than the trial rules were, and tighter for both drugs in the same two ways. Neither licence covers people carrying two copies of APOE4. And starting either drug is ruled out for anyone already taking an anticoagulant, the medicines that reduce clotting such as warfarin or apixaban (Eisai, 2026; Eli Lilly, 2026). That second point is often reported too bluntly. It bars starting treatment. If anticoagulation becomes necessary during a course, the Alzheimer's drug is paused, and it may be restarted only if the anticoagulation is no longer medically needed, following specialist review. Antiplatelet drugs such as aspirin sit outside that restriction and are allowed.
Because the licence is stricter than the trials were, plenty of people who get an Alzheimer's diagnosis wouldn't qualify even if the NHS were paying.
NHS availability
Neither drug is routinely available on the NHS in England, and as of September 2026 that has not changed.
Approval and funding are separate things. The first full approvals, in 2023 and 2024, were American. In the UK, the Medicines and Healthcare products Regulatory Agency approved lecanemab on 22 August 2024 (Medicines and Healthcare products Regulatory Agency, 2024a) and donanemab that October (Medicines and Healthcare products Regulatory Agency, 2024b). But a regulator judging a drug safe and effective doesn't mean the NHS will buy it.
That decision belongs to NICE. On 19 June 2025 it published final draft guidance on both drugs, concluding that the benefit, which it assessed as that delay of roughly four to six months, was too small to justify the price (National Institute for Health and Care Excellence, 2025). Both manufacturers appealed.
A third round of draft guidance followed. According to reporting in the Pharmaceutical Journal, it covered both drugs, was published on 31 March 2026, went out for consultation until 28 April, and was due back before the appraisal committee that June (Pharmaceutical Journal, 2026).
All of that is draft rather than final. Both appraisals remain in progress, neither has produced final published guidance, and neither drug is available for routine NHS use in the meantime (National Institute for Health and Care Excellence, 2026a, 2026b). Drafts can change. Funding is also decided separately in different parts of the UK, so Scotland goes through its own body, the Scottish Medicines Consortium, and the answer isn't automatically the same everywhere.
NICE isn't saying the science is wrong, and it has accepted that slowing the disease could count for something to patients and the people caring for them. Its judgement is that the size of that benefit, the uncertainty around it, and what delivering it would cost the health service don't add up to good enough value at the price being asked. Paying privately is possible, at considerable cost.
Risk reduction is a separate question
Everything above is about treating people who already have Alzheimer's disease. What follows is about something else, which is lowering the chance of developing dementia in the first place. The two have separate evidence bases, and findings about reducing future risk say nothing about treating a diagnosis someone already has.
Start with the conditions that complicate treatment, because they point somewhere useful. Heart and circulation problems, and blood pressure that isn't well controlled, raise the risk of harm from brain swelling enough to affect whether treatment is safe at all.
Several of those same conditions appear on the Lancet Commission's list of fourteen dementia risk factors that can be changed. High blood pressure, obesity and type 2 diabetes turn up on both (Livingston et al., 2024). The overlap is partial rather than exact and shouldn't be pushed too hard, but it is real. Looking after your heart, your circulation and your blood sugar helps your brain, whether or not you'd ever be a candidate for one of these drugs.
APOE4 sits in the same territory. Carrying it doesn't mean the changeable things stop being changeable, and nothing in the prevention evidence suggests inherited risk cancels out the rest. Your genes are fixed. Blood pressure and blood sugar aren't, although shifting them is rarely as simple as being told to (Livingston et al., 2024).
None of which means lifestyle replaces treatment, or that anyone who develops Alzheimer's just didn't try hard enough. The point is narrower. Several of the conditions that complicate treatment are the same ones that shape long-term brain health, and they repay attention in their own right.
The most-cited evidence that a structured programme can shift memory and thinking comes from the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability. Everyone calls it the FINGER trial.
It ran two years with 1,260 older adults at raised risk of dementia, none of whom had been diagnosed with it. Half got a structured programme of diet guidance, exercise, brain training and monitoring of heart and circulation risk, all delivered together. The other half got general health advice (Ngandu et al., 2015).
This one gets reported loosely, so here is what the trial actually found. Both groups improved on the cognitive tests. The structured group improved more, and the difference was real but small. A later analysis found the benefit held whether or not people were physically robust at the start (Pöyhönen et al., 2025).
What the trial reported was a modest difference in scores on a battery of cognitive tests. That is not the same as fewer people going on to develop Alzheimer's disease, which it did not show. Because all four parts of the programme were delivered together, nobody can say how much came from any single one of them, diet included. It does not establish effectiveness in people already diagnosed with Alzheimer's, nor that any particular commercial programme, here or anywhere else, prevents dementia.
On nutrition specifically, a 2026 study at the University of Kansas Medical Center looked at two omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in the blood of older adults whose memory and thinking were normal. Those with higher combined levels had less amyloid in the brain regions hit earliest in the disease (Christifano et al., 2026).
That was an observational snapshot. It can show that two things occur together in the same people, but not that one causes the other, and it says nothing about whether taking omega-3 supplements changes anything. It's a lead, and so far nothing more than a lead.
What it comes down to
For a narrow group of people with early Alzheimer's disease who meet the safety criteria, these drugs offer a modest slowing of decline on average. That has to be set against the risk of brain swelling, the scans and the fortnightly or monthly infusions, and the chance that treatment is interrupted or stopped early.
Whether any particular person is suitable is a question for a specialist, not for an article. And the evidence about lowering future dementia risk, which is where the second half of this piece has been, is a separate body of work from the evidence about treating a diagnosis someone already has. Neither one answers the other.
Where nutritional support fits
At You Nutrition Clinic, Dr Kirstie Lawton leads a team that includes Nicolle, a registered nurse and nutritional therapist with over 20 years’ experience in memory-clinic care and Alzheimer’s clinical trials.
For people concerned about memory changes, future risk or living with dementia, we take a comprehensive, systems-based approach. Clinical history, dietary assessment and targeted testing, including blood tests, nutrigenomics and metabolomics, help us explore metabolic regulation, nutrient status, gut function, hormonal influences and inflammatory markers.
These findings inform an individual nutrition and lifestyle programme, with ongoing support alongside your medical care.
Contact Nicolle to discuss your needs, or explore our cognitive health programmes.
🧩 Connect with us
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Stay curious. Stay hopeful. Support your brain. 🧠
Disclaimer: This article is for informational and educational purposes only and does not constitute medical advice. Always consult with a qualified, registered medical doctor (MD) for diagnosis and treatment decisions.
References
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