Summary: What the New Drugs Actually Do

They are sitting in a neurologist’s office, married forty-three years. The PET scan confirmed amyloid plaques. His symptoms are mild: forgotten appointments, lost conversational threads, repeated questions. He still drives, still manages the finances, still knows exactly who she is. He asks the question that matters most: “Will this fix it?”

The pause before she answers is the most important moment in the conversation.

For the first time in history, FDA-approved treatments can slow Alzheimer’s progression. Lecanemab and donanemab are monoclonal antibodies that target and clear amyloid beta from the brain. Both require confirmed amyloid pathology. Both work only in early-stage disease. The pivotal trial for lecanemab showed 27% less decline compared to placebo over eighteen months, roughly five to seven months of preserved cognitive time. Not a cure. Not a halt. But for a family holding onto every clear conversation, five to seven months is not nothing.

Donanemab showed similar results, with one additional feature: the possibility of stopping treatment once amyloid is sufficiently cleared. Most patients achieved amyloid-negative status within about eighteen months. Long-term data is still being gathered.

What these drugs cannot do: restore lost function, work in moderate or advanced disease, address tau pathology or neuroinflammation, or guarantee benefit for any individual patient. They are not cures. They are disease-modifying treatments that offer modest slowing in a subset of patients.

The risks are real. ARIA, amyloid-related imaging abnormalities, occurs in 13 to 35% of treated patients and can cause brain swelling or microbleeds. Most cases are asymptomatic and detected on monitoring MRI. A small percentage cause symptoms: headache, confusion, dizziness, visual changes. The risk is substantially higher for carriers of two copies of the APOE ε4 gene. Monitoring requires MRI scans every few months during treatment.

The costs are substantial. Lecanemab runs roughly $26,500 per year for the drug. Add PET scans, MRIs, infusion visits, and specialist appointments, and first-year costs can exceed $40,000. Medicare covers these treatments, but copays, travel, and time off work for caregivers add up. The infrastructure to deliver these treatments does not exist everywhere: PET scanners, infusion centers, and experienced neurologists are concentrated in metropolitan areas. Black and Hispanic Americans face the highest disease risk and the least access to treatment.

The pipeline behind these drugs is active. Trontinemab may offer faster amyloid clearance with fewer side effects. Anti-tau drugs are in clinical trials, with results expected between 2026 and 2028. GLP-1 agonists are being tested for Alzheimer’s. Prevention trials are asking whether treatment before symptoms can delay decline entirely. Effective combination therapy is likely a decade or more away.

For the family at the neurologist’s office: the benefits are real but modest, the risks are manageable for most people, and the decision belongs to you. For people not yet at the treatment decision: these drugs strengthen the case for early detection, because the window only opens early. For people with moderate or advanced disease: these drugs are not currently an option. That is a hard truth, and it deserves to be said directly.

The neurologist pauses, then says: “These drugs will not fix it. What they may do is slow it down. Buy time. Keep you closer to where you are now for longer.” That honesty is what this audience deserves.