Anti‑Amyloid Therapies for Alzheimer’s: How Lecanemab, Donanemab, and Emerging Drugs Work

Monoclonal‑antibody drugs such as lecanemab (Leqembi) and donanemab (Kisunla) bind to beta‑amyloid plaques in the brain, the hallmark lesions of Alzheimer’s disease. Clinical trials show they can reduce the rate of cognitive decline by roughly 20‑40 % in patients with early‑stage disease.

Alzheimer’s remains the leading cause of dementia in older adults in the United States. Although a cure is still elusive, current treatment strategies focus on symptom management and preserving quality of life.

Anti‑amyloid therapies represent a newer disease‑modifying approach. By targeting amyloid plaques directly, these agents aim to slow the underlying neurodegenerative process rather than merely alleviating symptoms. The field is still evolving, but the early data are encouraging.

Read on to understand the benefits, limitations, and practical considerations of anti‑amyloid treatment for Alzheimer’s disease.

Beta‑amyloid protein aggregates form extracellular plaques that disrupt neuronal communication and trigger cell death. The accumulation of these plaques is a central feature of Alzheimer’s pathology.

Anti‑amyloid drugs are engineered monoclonal antibodies that attach to beta‑amyloid, flagging it for clearance by the immune system. This mechanism can modestly slow disease progression and, in some trials, lessen cognitive decline by 20‑40 %.

The U.S. Food and Drug Administration (FDA) granted traditional approval to lecanemab in 2023 and to donanemab in 2024.

Both medications are administered intravenously by a healthcare professional. Lecanemab is given every two weeks, whereas donanemab is infused once every four weeks.

A prior FDA‑approved antibody, aducanumab (Aduhelm), was withdrawn from the market in 2024.

Emerging Anti‑Amyloid Therapies

Research continues to generate next‑generation anti‑amyloid candidates. Two of the most promising are remternetug—an optimized version of donanemab—and trontinemab, a reengineered form of the earlier investigational drug gantenerumab.

Conventional Alzheimer’s medications primarily address symptoms. In contrast, anti‑amyloid antibodies aim at the root cause—the plaques—offering the potential to alter disease trajectory. However, they are not curative and cannot reverse existing damage.

While the observed clinical effects are modest, anti‑amyloid agents constitute the most advanced therapeutic avenue for disease modification and remain a focal point of ongoing trials.

These treatments are most appropriate for individuals in the mild‑cognitive‑impairment (MCI) stage or early Alzheimer’s dementia. Amyloid deposition can begin up to two decades before clinical symptoms appear; once the disease advances, additional pathologies such as tau tangles dominate, and plaque‑focused therapy alone becomes insufficient.

Eligibility requires confirmation of amyloid burden, typically via amyloid PET imaging or cerebrospinal‑fluid analysis.

Common, mild adverse effects include:

• Headache
• Cough
• Diarrhea
• Nausea or vomiting
• Rash
• Infusion‑related reactions

The most serious risk is amyloid‑related imaging abnormalities (ARIA), which manifest as brain edema or microhemorrhage on MRI. ARIA is often asymptomatic but can cause headache, dizziness, or seizures, and in rare cases may be fatal. Continuous MRI monitoring is therefore essential.

Anti‑amyloid drugs are biologics, making them considerably more expensive than traditional symptomatic agents. Additional costs arise from required diagnostic scans (PET, MRI) and more frequent clinical visits.

Because lecanemab and donanemab are relatively new, biosimilar alternatives are not yet available. Out‑of‑pocket expenses will vary widely based on individual insurance coverage.

In summary, anti‑amyloid antibodies can modestly slow progression in early Alzheimer’s by clearing plaques, but they are not a cure. They require careful patient selection, monitoring for ARIA, and a clear discussion of cost.

Patients should consult their neurologist or memory‑clinic specialist to determine whether a currently approved anti‑amyloid drug—or enrollment in an experimental trial—fits their treatment plan.