Which Alzheimer’s treatments received FDA approval between 2020 and 2025 and what are their mechanisms?

1. Two new disease‑modifying approvals, and what they target

The FDA converted lecanemab (Leqembi; lecanemab‑irmb) from accelerated to traditional approval after a confirmatory trial verified clinical benefit; lecanemab is described as an amyloid‑beta directed antibody that clears protofibrils and plaques ^{[1] [3]}. Separately the FDA approved donanemab (branded Kisunla) for treatment of Alzheimer’s disease; donanemab is an anti‑amyloid antibody administered by IV infusion that reduced clinical decline vs placebo in a large Phase 3 study ^{[2] [5]}.

2. How these antibodies work — the shared mechanism

Both agents are monoclonal antibodies that bind pathological forms of beta‑amyloid in the brain and promote their removal, a strategy labelled “anti‑Aβ” or anti‑amyloid immunotherapy. Clinical write‑ups and regulatory documents specify that they reduce amyloid levels measured by PET and target protofibrillar or plaque forms of Aβ, with clinical trials using biomarkers to show target engagement ^{[3] [2] [4]}.

3. Clinical benefit: modest but statistically significant slowing

Regulatory summaries report that donanemab showed statistically significant reductions in clinical decline on integrated scales (iADRS, ADAS‑Cog13, ADCS‑iADL) at Week 76 in a 1,736‑patient randomized trial ^[2]. Lecanemab’s approval followed a confirmatory Phase 3 endpoint that regulators interpreted as verification of clinical benefit; public summaries and advocacy groups characterize the magnitude as a slowing of progression for people with early disease ^{[1] [3]}.

4. Who the FDA says should receive these drugs

Labeling and FDA statements restrict initiation to people with mild cognitive impairment or mild dementia due to Alzheimer’s disease — the populations studied in trials — and require confirmation of elevated brain amyloid before treatment ^{[1] [2] [5]}. FDA and clinical reviews emphasize there are no safety or effectiveness data for starting treatment at earlier or later stages than those studied ^{[1] [2]}.

5. Safety and monitoring caveats highlighted by regulators

The approvals and review literature stress the role of biomarkers and monitoring: amyloid PET or cerebrospinal fluid tests were used to confirm target presence, and PET was used to measure treatment‑related amyloid reduction in trials ^{[2] [4]}. Available sources do not mention detailed adverse‑event rates beyond trial efficacy statements; labeling and FDA summaries imply safety monitoring is part of post‑approval use but specific numbers are not provided in these excerpts ^{[1] [2]}.

6. Broader context — why amyloid antibodies dominated 2020–2025

Multiple reviews and pipeline analyses position anti‑amyloid monoclonals as the leading disease‑targeting advances through 2025, noting that approvals depended on biomarker‑driven programs and that the pipeline remains diverse (amyloid, tau, inflammation, neurotransmitter targets) with many trials ongoing ^{[4] [6] [7]}. NIH and professional reviews frame these approvals as an important scientific milestone while calling for more research on optimal use, populations, and combinations with other approaches ^{[8] [9]}.

7. Alternative viewpoints and limitations in the record

Some scientific commentary and pipeline overviews caution that amyloid removal has not delivered dramatic cures and that effect sizes are modest; they call for combination therapies and broader mechanism exploration ^{[10] [11]}. Regulatory texts and reviews note that approvals were contingent on biomarker evidence and confirmatory trials, showing regulators required stronger proof than earlier accelerated pathways ^{[1] [4]}. Available sources do not mention approvals of non‑amyloid disease‑modifying drugs in this period or specific numeric effect‑size comparisons beyond the snippets cited (not found in current reporting).

8. What this means for patients and clinicians now

For clinicians and patients the practical takeaway from 2020–2025 is that two anti‑amyloid monoclonal antibodies are FDA‑approved for early Alzheimer’s with biomarker confirmation and have demonstrated slowing of decline in trials; access, safety monitoring, and patient selection remain active areas of implementation and research according to NIH and advocacy organizations ^{[2] [3] [8]}. Reported developments in 2025 also include dosing/administration changes (e.g., maintenance dosing options for lecanemab) that aim to broaden practical use, though implementation details vary by product ^{[3] [12]}.

If you want, I can assemble a one‑page comparison table with dosing schedules, trial sizes, and the exact trial endpoints cited in the FDA summaries above (using the same sources).