Donanemab slows Alzheimer's by 35%, but doctors split on cost-benefit

A neurologist in Lisbon sits across from a patient in the early stages of Alzheimer's disease and mentions a new option: a drug called Donanemab that might slow what's coming. It arrived in Portugal this spring, approved by regulators and administered for the first time on April 20th at a private clinic network called Campus Neurológico. The drug works by targeting the beta-amyloid plaques that accumulate in the brain and choke off neurons. Clinical trials showed it can delay cognitive decline by 35 to 40 percent over eighteen months of treatment. But there's a catch, and it's a substantial one: the full course costs around 40,000 euros, and Portugal's public health system hasn't agreed to pay for it yet.

Donanemab is a monoclonal antibody manufactured by Lilly, approved by European regulators in July 2025 and by Portugal's drug authority, Infarmed, that September. The drug binds to beta-amyloid and activates the brain's immune cells—microglia—to clear the plaques away. A major clinical trial called TRAILBLAZER enrolled roughly 1,700 patients, split between those receiving the actual drug and those getting a placebo. After eighteen months, patients on Donanemab saw their cognitive scores decline by eleven points on a standardized assessment scale, compared to thirteen points in the placebo group. The treatment also slowed the deterioration of patients' ability to perform basic daily tasks by about 40 percent. Ana Castro Caldas, a neurologist and clinical director at Campus Neurológico, calls it revolutionary—a disease-modifying therapy that changes how we think about Alzheimer's treatment. The goal, she explains, is to keep patients autonomous and functional for longer, delaying the point at which they need constant help managing medications, finances, and personal care.

Yet the medical community is fractured on whether the investment makes sense. Luísa Alves, a neurologist at Hospital Egas Moniz in Lisbon, points to a hard reality: the benefit lasts only four to seven months after treatment ends. The drug doesn't improve symptoms; it merely slows their worsening. For that modest gain, she argues, the cost is unjustifiable. She advocates instead for non-pharmacological interventions—cognitive stimulation, physical exercise, management of vascular risk factors, healthy diet, and social engagement—which have proven effective in early-stage cognitive decline and cost far less. The UK's National Institute for Health and Care Excellence reached a similar conclusion in late 2024, declaring that Donanemab offered only minimal benefit and was five to six times more expensive than the NHS considers acceptable. Helen Knight, the agency's director of medicine evaluation, stated plainly: the benefit simply doesn't justify the cost.

The safety profile adds another layer of concern. In the TRAILBLAZER trial, roughly one-third of patients experienced brain swelling, usually without lasting harm. But two volunteers died, and some patients suffered cerebral hemorrhages. When monoclonal antibodies work to remove amyloid plaques, they can increase the permeability of blood vessel walls, raising the risk of brain edema and microhemorrhages. Castro Caldas notes that most cases are asymptomatic and reversible, and that frequent MRI monitoring during treatment can catch problems early. She also suggests Donanemab may be slightly safer than its competitor, Lecanemab, another monoclonal antibody approved for Alzheimer's. Still, the drug carries significant contraindications: it's not suitable for patients with poorly controlled high blood pressure, prior brain hemorrhage, multiple microhemorrhages, or those taking anticoagulants. Alves emphasizes that many patients cannot begin these therapies at all because of such restrictions.

There's also a timing problem. These drugs work only in early-stage disease, when beta-amyloid and tau proteins are accumulating but cognitive symptoms are still mild. Yet diagnosis at that stage is difficult and often delayed. Patients typically start with their family doctor, who may not immediately suspect Alzheimer's, especially in younger patients. Some are prescribed antidepressants before eventually reaching a neurologist. Once diagnosed, reactions vary widely. Some patients feel relief—finally, a name for what's been troubling them. Others deny the diagnosis entirely, a condition neurologists call anosognosia. Alves notes that many patients refuse to accept they're ill, resist involving family members in appointments, and come to consultations only because relatives insist. The stigma around Alzheimer's remains powerful, and acceptance of the diagnosis is crucial to treatment adherence.

Castro Caldas defends the investment in Donanemab, arguing that until now, doctors have had little to offer beyond medications that might marginally improve memory or attention while the disease continues its course. A disease-modifying therapy, even one with modest gains, represents a genuine shift. But Alves counters that the money would be better spent on subsidizing gym memberships and cognitive training programs—interventions that are cheaper, accessible to more people, and supported by evidence. The question of whether Infarmed will fund Donanemab through Portugal's public health system remains open. The agency is conducting a pharmacoeconomic evaluation, but no timeline has been announced. For now, only patients who can afford 40,000 euros out of pocket can access the drug. Campus Neurológico has treated one patient and plans to begin three more, all between 65 and 80 years old. The treatment requires frequent monitoring with MRI scans and PET imaging to track amyloid reduction, adding to the burden and expense. Whether this new option will become standard care or remain a luxury for the wealthy depends on decisions still being made.