Reviewed by the Help Dementia Editorial Team — our editors review every article for accuracy against guidance from the National Institute on Aging, the Alzheimer’s Association, and peer-reviewed sources.
Research culminates sits at the center of this dementia and brain health question.
After more than a decade of intensive research and clinical trials, two disease-modifying drugs have received FDA approval for Alzheimer’s disease, offering the first genuine hope for slowing cognitive decline in the early stages of the illness. Leqembi (lecanemab) and Kisunla (donanemab) represent a fundamental shift in how doctors approach Alzheimer’s treatment—moving from temporary symptom management to addressing the underlying biological processes that drive neurodegeneration. For families facing an Alzheimer’s diagnosis, this represents a critical turning point in the disease’s trajectory. The first of these treatments, Leqembi, received full FDA approval in July 2023 and has already demonstrated measurable benefits in clinical settings.
A 64-year-old diagnosed with early cognitive decline from Alzheimer’s who began Leqembi treatment showed a 64% likelihood of experiencing at least a 25% slowing of cognitive decline over the study period. While these numbers may seem modest on the surface, they represent the difference between losing significant independence within a year versus maintaining that independence for several additional years. The approval of Kisunla in July 2024 further validates this new treatment paradigm and provides patients with additional options based on their individual circumstances and risk profiles. What makes this moment particularly significant is that both drugs work by clearing the toxic amyloid plaques that accumulate in the brains of Alzheimer’s patients—addressing the root cause rather than simply treating symptoms.
Table of Contents
- What Are the New FDA-Approved Alzheimer’s Disease-Modifying Treatments?
- How Do These Disease-Modifying Drugs Actually Work and What Are Their Limitations?
- Who Can Actually Benefit from These New Treatments?
- Navigating Treatment Options and Administration Methods
- Understanding Safety Concerns and Side Effects of Anti-Amyloid Therapy
- The Expanding Pipeline of Future Alzheimer’s Treatments
- The Role of Early Detection in Making New Treatments Work
- Conclusion
What Are the New FDA-Approved Alzheimer’s Disease-Modifying Treatments?
Leqembi (lecanemab) became the first monoclonal antibody approved for Alzheimer’s disease, and its approval followed decades of research into the amyloid hypothesis—the theory that accumulation of beta-amyloid protein in the brain triggers the cascade of neurodegeneration seen in Alzheimer’s. In clinical trials lasting 18 months, participants taking Leqembi demonstrated approximately a 5.3-month delay in cognitive decline compared to those receiving placebo. This means that someone expected to progress significantly over 18 months might instead maintain roughly five additional months of cognitive function and independence. Beyond the initial clinical trials, Leqembi’s approval pathway has continued to evolve. In January 2025, the FDA approved a maintenance dosing schedule of once every four weeks, making the treatment more practical for patients to manage.
Even more significantly, in August 2025, the FDA approved Leqembi IQLIK, a once-weekly subcutaneous self-administered injection. This advancement addresses one of the major barriers to treatment adoption—many patients previously needed to visit an infusion center every two weeks, a significant logistical challenge for those with early cognitive decline. Kisunla (donanemab), approved just one year after Leqembi, showed comparable effectiveness in slowing disease progression. In its clinical trials, Kisunla demonstrated approximately 35% slower disease progression over 18 months compared with placebo, which translates to a delay of roughly 4.5 to 7.5 months in symptom progression. Like Leqembi, Kisunla targets amyloid plaques in the brain, though it uses a slightly different mechanism of action that may make it suitable for patients who don’t tolerate Leqembi well.
How Do These Disease-Modifying Drugs Actually Work and What Are Their Limitations?
Both Leqembi and Kisunla belong to a class of drugs called monoclonal antibodies, which are engineered proteins designed to recognize and bind to specific targets in the body. In this case, they target amyloid-beta, the sticky protein that accumulates into plaques between nerve cells in the brains of Alzheimer’s patients. When the antibody binds to these plaques, it essentially flags them for the immune system to clean up and remove, reducing the toxic burden on the brain. However, these drugs come with important limitations that patients and families need to understand. First, both medications work best when administered in the early stages of cognitive decline—what researchers call the “mild cognitive impairment” or early symptomatic phase. They are not approved for advanced Alzheimer’s disease, and evidence suggests they provide minimal benefit once significant brain damage has already occurred.
Second, while a 5.3-month delay in decline sounds meaningful, it’s important to recognize that these drugs do not stop Alzheimer’s progression entirely. They slow it down, but patients will still eventually experience cognitive decline. Third, both medications carry a risk of amyloid-related imaging abnormalities (ARIA), which means some patients develop microhemorrhages or microinfarcts visible on brain imaging. While most cases are asymptomatic, this represents a genuine safety consideration that requires ongoing monitoring. The most significant limitation is also the most practical one: these medications require either regular infusions at medical centers or injections that demand careful technique. For patients with early cognitive decline, managing the logistics of treatment can become its own challenge. Some patients may also struggle with the cost; while Medicare typically covers Leqembi and Kisunla, the medications are expensive, and co-pays can still represent a substantial financial burden for families.
Who Can Actually Benefit from These New Treatments?
The FDA-approved indications for both Leqembi and Kisunla specify that they are intended for patients with mild cognitive impairment or mild dementia stage of disease due to Alzheimer’s disease, and who have documented evidence of amyloid pathology. This means that not every person with an Alzheimer’s diagnosis is eligible. A person in the moderate or advanced stages of Alzheimer’s would not benefit from these treatments based on current evidence, nor would someone who has not had imaging or biomarker evidence confirming amyloid accumulation in their brain. This eligibility requirement highlights why biomarker testing has become increasingly important. A 72-year-old woman experiencing memory problems might get a PET scan showing significant amyloid accumulation in her brain—making her an ideal candidate for Leqembi or Kisunla.
By contrast, an 75-year-old man with similar symptoms but without documented amyloid pathology might have a different underlying cause for his cognitive decline, meaning these medications wouldn’t be appropriate for him. Age itself is not a barrier; what matters is the stage of disease and confirmation of amyloid pathology. The AHEAD Study, currently underway, is testing whether Leqembi might eventually be appropriate for asymptomatic people who have amyloid accumulation in their brains but haven’t yet developed cognitive symptoms. If this research proves successful, it could eventually expand the population who might benefit from treatment to include cognitively normal older adults at high risk for Alzheimer’s. Such preventive treatment would represent a major paradigm shift in how we approach the disease.
Navigating Treatment Options and Administration Methods
The evolution of Leqembi administration options illustrates how treatment accessibility is improving. The original Leqembi infusions required patients to visit an infusion center every two weeks, a significant commitment for someone with early cognitive decline who might struggle with transportation or anxiety about medical procedures. The approval of once-every-four-weeks maintenance dosing in January 2025 cut the number of clinic visits in half. Then, in August 2025, the subcutaneous self-administered injection option became available, potentially allowing patients to give themselves Leqembi at home once weekly. For a patient deciding between Leqembi and Kisunla, the choice often comes down to practical and individual factors.
Kisunla is still typically administered as an intravenous infusion at medical centers, though dosing may be less frequent than the original Leqembi schedule. A patient with reliable transportation and strong social support might find either option manageable, while someone who is homebound or lives far from a medical center might strongly prefer the new subcutaneous Leqembi injection. Both medications require ongoing monitoring for safety, including periodic amyloid PET imaging or MRI scans to check for imaging abnormalities. The expanding array of administration methods also reflects the reality that there is no one-size-fits-all approach to Alzheimer’s treatment. A working professional with flexible scheduling might handle monthly infusions easily, while a retired person living alone might prefer weekly self-injection. These practical considerations matter significantly for treatment adherence and long-term outcomes.
Understanding Safety Concerns and Side Effects of Anti-Amyloid Therapy
The most significant safety concern associated with both Leqembi and Kisunla is amyloid-related imaging abnormalities (ARIA), which occur when the process of clearing amyloid plaques from the brain triggers inflammation and microhemorrhages or microinfarcts. In clinical trials, a meaningful percentage of patients developed these imaging abnormalities—though most remained asymptomatic. Some patients, however, experienced cognitive symptoms, headaches, confusion, or vision changes attributable to ARIA, and a small number required hospitalization or had their treatment discontinued. This safety profile underscores why these medications are not appropriate for everyone. Patients taking blood thinners like warfarin face higher risk of complications from ARIA, making them less suitable candidates.
Patients with advanced cerebral amyloid angiopathy, a condition involving amyloid deposits in blood vessel walls, similarly face higher risk. These patients need careful evaluation before starting anti-amyloid therapy, and some may be advised against treatment entirely based on their individual risk profile. Regular monitoring is essential for anyone on Leqembi or Kisunla. This typically includes periodic MRI or PET imaging to detect ARIA before symptoms develop, as well as ongoing clinical assessment for any emerging cognitive or neurological symptoms. For some patients, this monitoring burden—combined with the safety considerations—makes a careful risk-benefit discussion with their neurologist essential before starting treatment.
The Expanding Pipeline of Future Alzheimer’s Treatments
While Leqembi and Kisunla represent the first generation of disease-modifying treatments for Alzheimer’s, they are far from the final chapter of drug development for the disease. According to the latest data from UC San Francisco, there are currently 138 different drugs in clinical development across 182 clinical trials specifically targeting Alzheimer’s disease. This represents an unprecedented level of investment and scientific attention to the disease. The pipeline is diverse in its approach. Approximately 30% of drugs in development are biological therapies targeting underlying disease mechanisms like amyloid or tau.
About 43% are small molecule drugs that could potentially be taken as pills rather than infusions or injections. Another 14% focus on cognitive enhancement, attempting to improve thinking and memory function directly, while 11% target neuropsychiatric symptoms like depression, anxiety, and behavioral changes that often accompany Alzheimer’s. This diversity means that even if a patient doesn’t tolerate or benefit from Leqembi or Kisunla, other options may eventually become available. One particularly promising drug in development is Trontinemab from Roche. Early Phase III trial data showed that 92% of participants who received Trontinemab had no measurable amyloid plaques on brain imaging after 28 weeks of treatment—a stunning result if confirmed. The full Phase III trials, TRONTIER 1 and 2, are ongoing with results expected in 2028, suggesting that even more effective anti-amyloid drugs may be coming to market within the next few years.
The Role of Early Detection in Making New Treatments Work
Perhaps the most important factor in whether these new treatments will significantly impact Alzheimer’s at the population level is early detection. These drugs work best in the earliest stages of cognitive decline, when amyloid has accumulated but the brain has not yet undergone extensive tau tangles and neuronal death. By the time someone reaches advanced dementia stages, clearing amyloid plaques does little good because too much irreversible damage has already occurred.
This has sparked growing interest in biomarker testing—particularly blood tests that can detect early signs of Alzheimer’s pathology before cognitive symptoms appear. A breakthrough example is the p-tau217 protein test, which can predict Alzheimer’s symptom onset within approximately 3–4 years in cognitively normal individuals with amyloid accumulation in their brains. If these biomarker tests become part of routine cognitive screening for older adults, it could shift the paradigm from treating symptomatic disease to preventing symptomatic disease entirely. Someone might receive a blood test showing elevated p-tau217 and amyloid accumulation, get confirmed with advanced imaging, and begin treatment while still cognitively normal—similar to how we treat high blood pressure or high cholesterol before they cause a heart attack.
Conclusion
The approval of Leqembi and Kisunla marks the culmination of more than a decade of intensive Alzheimer’s research and represents the first genuine disease-modifying treatments for this devastating illness. These medications can slow cognitive decline by approximately 5 to 7 months in people with early symptomatic disease—a meaningful difference that can help preserve independence, maintain quality of life, and allow more time with family. Critically, they address the underlying amyloid pathology rather than simply masking symptoms, validating decades of research into the biological mechanisms of Alzheimer’s disease.
However, these treatments are not a cure, and they come with important limitations and safety considerations. They work best in early disease stages, they require careful patient selection and monitoring, and they do not stop Alzheimer’s progression entirely. The real promise of the coming decade lies not just in these initial treatments, but in the 138 additional drugs in clinical development, the expansion of biomarker testing for early detection, and the potential to eventually treat Alzheimer’s before symptoms ever appear. For individuals and families currently facing an Alzheimer’s diagnosis, discussing eligibility for Leqembi or Kisunla with a neurologist or memory specialist is an important conversation—one that could significantly impact the disease’s trajectory.
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For more, see NIH MedlinePlus — cognitive testing.
