The new Alzheimer’s antibody drugs — lecanemab (Leqembi) and donanemab (Kisunla) — represent the first treatments in history that actually slow the progression of Alzheimer’s disease rather than just easing symptoms. That is a genuine milestone. But these drugs also come with significant risks, high costs, and a level of benefit that remains actively debated among neurologists. For families weighing options for a loved one in the early stages of Alzheimer’s, the honest answer is that these drugs offer real but modest benefits alongside real and sometimes serious risks.
Both drugs work by targeting amyloid plaques — the protein clusters in the brain long associated with Alzheimer’s disease. Clinical trials showed lecanemab slowed progression by roughly 27% and donanemab by approximately 29% over 18 months, measured on standardized cognitive scales. To put that in concrete terms: on an 18-point cognitive decline scale, lecanemab users declined 0.45 points less than placebo over a year and a half. That translates to more months of independent daily functioning — being able to manage finances, remember appointments, drive — before those abilities fade. This article covers what the clinical trial data actually shows, who these drugs are appropriate for, what the serious risks look like, and how to think through whether treatment makes sense for a specific patient.
Table of Contents
- How Do the New Alzheimer’s Antibody Drugs Actually Work — and What Do the Trials Show?
- What Are the Real Benefits of Lecanemab and Donanemab for Patients and Families?
- What Are the Serious Risks — and How Common Are They?
- How Much Do These Drugs Cost — and Who Pays?
- Who Should and Should Not Consider These Treatments?
- Why Are Neurologists Divided on These Drugs?
- What Does the Future of Alzheimer’s Antibody Treatment Look Like?
- Conclusion
- Frequently Asked Questions
How Do the New Alzheimer’s Antibody Drugs Actually Work — and What Do the Trials Show?
Lecanemab and donanemab are monoclonal antibodies, meaning they are laboratory-engineered proteins that bind to specific targets in the body. In this case, both drugs bind to amyloid beta — the protein that aggregates into plaques in the brains of Alzheimer’s patients. By clearing these plaques, the drugs aim to interrupt one of the central processes believed to drive Alzheimer’s progression. Both received FDA approval as disease-modifying treatments, a designation that had eluded Alzheimer’s medicine for decades. The trial data is specific: in the lecanemab trial, patients on the drug showed 27% less cognitive decline over 18 months compared to those on placebo. Donanemab showed 29% slowing in a similar timeframe. These numbers sound compelling, but context matters.
The underlying scale used for lecanemab — the Clinical Dementia Rating Sum of Boxes — runs from 0 to 18. The 27% improvement translated to 0.45 fewer points of decline. Critics have raised legitimate questions about whether a difference that small is noticeable in daily life. Supporters counter that even a modest delay in early-stage decline buys meaningful time for patients and families. Both positions reflect reasonable readings of the same data. It is also worth noting that both drugs are approved only for early-stage Alzheimer’s — mild cognitive impairment or mild dementia — where amyloid plaques are confirmed present. They are not intended for moderate or advanced disease. A patient whose diagnosis was made years ago and whose condition has significantly progressed would not be a candidate.
What Are the Real Benefits of Lecanemab and Donanemab for Patients and Families?
The most meaningful benefit these drugs offer is time — specifically, more time in the earlier, more functional stages of the disease. Alzheimer’s progression is not linear, but the early stages, when a person can still live semi-independently, hold a job, or maintain meaningful relationships, are qualitatively different from later stages. Delaying the transition to more severe impairment, even by several months, has practical consequences for patients and caregivers. Stanford Health Care notes that patients retaining more capacity for daily activities represents a genuine quality-of-life gain, even if it is difficult to quantify precisely. On the administration front, access has improved.
As of January 2025, the FDA approved a once-every-four-weeks maintenance dosing schedule for lecanemab, down from more frequent infusions. A subcutaneous injection option was also approved later in 2025, which removes the need for intravenous infusion entirely for eligible patients. For someone receiving treatment for 18 months or longer, these changes meaningfully reduce the logistical burden on patients and families. There is also emerging data on high-risk populations. An October 2025 study found that lecanemab and donanemab may provide benefit even for carriers of the APOE4 gene — a genetic variant that significantly increases Alzheimer’s risk. This matters because APOE4 carriers were previously considered a more complicated population to treat, and this finding, while still being examined, is cautiously encouraging.
What Are the Serious Risks — and How Common Are They?
The most serious risk associated with both drugs is a condition called ARIA — amyloid-related imaging abnormalities. This refers to brain swelling (edema) and small bleeds (microhemorrhages) that show up on MRI scans. In lecanemab trials, 17.3% of drug recipients showed ARIA compared to 9% on placebo. The numbers with donanemab were more striking: up to 30.5% of donanemab patients showed brain abnormalities versus 0.8 to 7.2% in the placebo group. Overall, the relative risk of ARIA for patients on these drugs is approximately 4.35 times higher than for those on placebo. In most cases, ARIA does not cause symptoms and resolves on its own or with a pause in treatment.
But not always. Three deaths in clinical trials were attributed to ARIA in the donanemab trial — a fact that does not appear often in promotional materials but is documented in peer-reviewed literature. For a healthy 72-year-old in early-stage Alzheimer’s, the risk calculus looks different than it does for someone with existing cardiovascular disease or a history of strokes. APOE4 gene carriers face elevated ARIA risk on top of their already elevated disease risk. Homozygous APOE4 carriers — those who inherited the gene from both parents — are at particularly high risk. Genetic testing prior to treatment is now standard in most protocols, and some clinicians advise against treatment for homozygous APOE4 carriers given the compounded risk picture.
How Much Do These Drugs Cost — and Who Pays?
Cost is not a minor footnote. Lecanemab runs approximately $26,500 per year; donanemab approximately $32,000 per year. Those figures cover the drug alone. Required brain imaging — PET scans to confirm amyloid presence before starting treatment, and repeated MRIs to monitor for ARIA during treatment — adds several thousand dollars more annually. For a patient receiving treatment over two to three years, the total cost can easily exceed $100,000. Medicare covers lecanemab for eligible patients who meet specific criteria, including confirmed amyloid pathology and enrollment in a data registry. But coverage is not seamless or guaranteed.
Access varies by geography, specialist availability, and whether the treating physician has the infrastructure to manage monitoring requirements. Many patients in rural areas or without access to academic medical centers face real barriers even if they are medically appropriate candidates. A Feb. 2024 survey of 75 neurologists found fewer than half recommended lecanemab to their patients, with insurance and coverage issues cited alongside limited satisfaction with the available data and the logistical demands of infusion-based treatment. The comparison between the two drugs on cost and administration is also worth noting. Donanemab, at roughly $32,000 per year, is more expensive than lecanemab. However, donanemab trials suggested that some patients who cleared their amyloid burden could potentially stop treatment — an outcome that has no parallel with lecanemab, where treatment is ongoing. Whether this translates to long-term cost savings in practice remains to be seen.
Who Should and Should Not Consider These Treatments?
The approved indication is specific: early Alzheimer’s disease with confirmed amyloid pathology, mild cognitive impairment, or mild dementia stage. Patients must receive a diagnosis from a specialist, typically a neurologist or geriatric psychiatrist, and must undergo amyloid PET imaging or cerebrospinal fluid testing to confirm amyloid is actually present. Not everyone with memory complaints or even a clinical Alzheimer’s diagnosis will have the amyloid burden these drugs target. Beyond the diagnostic requirements, several factors make some patients poor candidates. Those on blood thinners face elevated risk of serious bleeding from ARIA. Patients with a history of stroke, cerebral microbleeds, or other vascular brain disease are also at substantially higher risk of serious ARIA events.
Homozygous APOE4 carriers require especially careful risk-benefit discussion. Age alone is not a disqualifying factor, but frailty and overall health status matter in assessing whether potential cognitive benefit outweighs treatment risks. There is also a practical question of patient and family goals. For some families, the prospect of additional months of independence and functional capacity is worth navigating complex treatment, frequent MRIs, and infusion visits. For others — particularly those managing caregiving from a distance, or patients who find medical settings distressing — the treatment burden may outweigh the benefit. Neither choice is wrong. These are drugs that genuinely require individualized decision-making.
Why Are Neurologists Divided on These Drugs?
Despite FDA approval, physician enthusiasm has been notably measured. The 2024 survey of neurologists found that fewer than half were recommending lecanemab to patients — an unusual situation for a newly approved drug in a disease with so few treatment options. The reasons cited were a mix of practical and scientific: limited satisfaction with the scale of demonstrated benefit, concerns about ARIA management, insurance and prior authorization difficulties, and the logistical demands of infusion treatment and monitoring.
Some neurologists have published pointed criticisms arguing that the statistical benefit — fractions of a point on cognitive scales over 18 months — does not meet the threshold for clinical meaningfulness. Others argue that framing the benefit that way misses the forest for the trees, and that any delay in Alzheimer’s progression is worth pursuing given the absence of alternatives. The debate is ongoing, and families seeking specialist opinions may encounter genuinely differing recommendations from qualified physicians. Getting a second opinion from an academic medical center with Alzheimer’s disease research programs is reasonable.
What Does the Future of Alzheimer’s Antibody Treatment Look Like?
These drugs are likely the beginning of a treatment category, not the final word. Research into combination approaches — pairing amyloid-clearing antibodies with drugs targeting tau tangles, neuroinflammation, or other Alzheimer’s pathways — is underway. The hope is that combining mechanisms will produce more substantial slowing, or eventually halt progression altogether in some patients.
Administration is also likely to improve. The shift from biweekly infusions to monthly maintenance dosing and now subcutaneous injections for lecanemab tracks a pattern seen with other biologic drugs — initial approval for infusion, followed by more convenient delivery methods as post-approval data matures. Improved biomarker testing, including blood-based amyloid tests that could replace expensive PET scans, is advancing rapidly and could make the diagnostic pipeline more accessible and affordable within the next few years.
Conclusion
The new Alzheimer’s antibody drugs — lecanemab and donanemab — mark genuine scientific progress. They are the first treatments to slow Alzheimer’s progression rather than merely manage symptoms, and for appropriately selected patients in early stages of the disease, they offer real if modest benefits: more time in functional stages, more months of independence. That matters to patients and families. At the same time, these drugs carry serious risks, particularly brain swelling and bleeding that affect a meaningful percentage of patients.
They are expensive, logistically demanding, and not universally accessible. Neurologists remain divided on whether the scale of benefit justifies routine use. The right decision depends on the individual patient — their disease stage, genetic risk profile, overall health, access to monitoring, and personal priorities. For families navigating this decision, the most important step is a detailed, unhurried conversation with a specialist who can review the full picture.
Frequently Asked Questions
Are lecanemab and donanemab approved by the FDA?
Yes. Both have received full FDA approval as disease-modifying treatments for early Alzheimer’s disease with confirmed amyloid pathology. Lecanemab was approved under the brand name Leqembi; donanemab under the brand name Kisunla.
What is ARIA, and should it worry me?
ARIA stands for amyloid-related imaging abnormalities — essentially brain swelling and small bleeds detected on MRI. It occurred in 17.3% of lecanemab patients and up to 30.5% of donanemab patients in trials. Most cases are asymptomatic and resolve, but some are serious, and three deaths in the donanemab trial were attributed to ARIA. Regular MRI monitoring is required during treatment.
Does Medicare cover these drugs?
Medicare covers lecanemab for eligible patients who meet specific criteria, including amyloid confirmation and enrollment in a data registry. Coverage is not automatic and varies in practice; insurance logistics were cited as a barrier by neurologists in a 2024 survey.
Can people with the APOE4 gene take these drugs?
APOE4 carriers can receive these treatments, but face higher ARIA risk, particularly homozygous carriers who inherited the gene from both parents. Recent 2025 data suggests these patients may still receive benefit from treatment, but the risk-benefit conversation requires careful specialist guidance.
Do these drugs stop Alzheimer’s progression or reverse it?
Neither. These drugs slow progression by approximately 25-30% in early-stage disease. They do not stop the disease, and no symptomatic improvement is claimed. Cognitive decline continues, but at a somewhat slower rate.
What happens if a patient cannot access infusion centers?
Access is a real barrier, particularly in rural areas. However, a subcutaneous injection option for lecanemab was approved in 2025, which may improve access for patients without proximity to infusion facilities. Ongoing advocacy from the Alzheimer’s Association is pushing for broader coverage and access improvements.
