For years, the diagnosis of Alzheimer’s disease has felt like a one-way street, a relentless march of cognitive decline with no real detours or off-ramps. We’ve had medicines, sure, but they’ve largely focused on managing symptoms, offering a temporary reprieve rather than addressing the underlying cause. That’s why the full approval of anti-amyloid monoclonal antibodies like donanemab (marketed as Kisunla) and lecanemab (known as Leqembi) in 2026 marks such a monumental shift. These aren’t just incremental improvements; they represent a genuine breakthrough, offering the first real hope for moderately slowing the progression of early-stage Alzheimer’s. It’s a game-changer, plain and simple, and understanding the nuances of donanemab vs. lecanemab is absolutely vital for anyone grappling with this diagnosis.

As someone who’s spent years in education, observing firsthand the impact of cognitive challenges on individuals and families, I can tell you that this isn’t just medical news; it’s deeply personal news for millions. The ability to maintain independence and quality of life for longer isn’t just a clinical outcome; it’s a profound human aspiration. But with this hope comes a fresh set of questions, particularly around which treatment might be the right fit, the costs involved, and how our healthcare systems are preparing for widespread accessibility. Let’s dig into what these new treatments mean and how they stack up against each other.

1. The Amyloid Hypothesis: The Core of Both Treatments

To understand donanemab vs. lecanemab, you first have to grasp the central idea behind them: the amyloid hypothesis. For decades, scientists have theorized that the accumulation of sticky protein fragments called beta-amyloid in the brain is a primary driver of Alzheimer’s disease. These fragments clump together to form plaques, which are thought to disrupt communication between brain cells, eventually leading to their death and the cognitive decline we associate with Alzheimer’s.

Both donanemab and lecanemab are designed to target and clear these amyloid plaques. They are monoclonal antibodies, which means they are lab-made proteins that mimic your body’s own immune system. Essentially, they act like highly specialized guided missiles, seeking out and attaching themselves to beta-amyloid proteins, signaling the body to remove them. It’s a direct attack on what many believe is the root cause of the disease, rather than just patching up the symptoms.

While the amyloid hypothesis has been the dominant theory for a long time, it’s important to remember that science is always evolving. There are other contributing factors to Alzheimer’s, like tau tangles, inflammation, and vascular issues. However, the success of these anti-amyloid therapies strongly validates the idea that amyloid accumulation is a critical early step in the disease process. Removing these plaques early enough seems to create a window where the brain can function better for longer. This targeted approach represents a significant leap from previous treatments that mostly just tried to boost neurotransmitters or manage behavioral symptoms without tackling the underlying pathology.

2. Donanemab (Kisunla): Eli Lilly’s Powerful Contender

Let’s start with donanemab, manufactured by Eli Lilly and marketed as Kisunla. This drug has certainly turned heads in the medical community. Clinical trials have shown some truly impressive results, particularly for patients in the early stages of Alzheimer’s. We’re talking about a reduction in cognitive and functional decline by up to 35% over 18 months. Think about that for a moment: over a year and a half, patients experienced more than a third less decline than those on a placebo. That’s not a cure, but it’s a significant slowdown, giving people precious time.

Perhaps even more striking is donanemab’s efficacy in clearing amyloid plaques. On average, patients treated with donanemab saw an 84% reduction in amyloid plaques. That’s a near-total clearance for many. This high level of plaque removal is a key differentiator and suggests a potent mechanism of action. The idea is that by aggressively clearing these plaques, the drug can significantly impede the disease’s progression.

The clinical trial results for donanemab came from the TRAILBLAZER-ALZ 2 study, a global, randomized, double-blind, placebo-controlled Phase 3 trial. This study design is the gold standard for proving a drug’s effectiveness and safety. What made donanemab’s results particularly compelling was that the benefit was observed across different subgroups, including those with varying levels of tau pathology at baseline. Tau tangles are another hallmark of Alzheimer’s, and the fact that donanemab showed benefits even with existing tau pathology suggests a broader impact on the disease cascade, even if indirectly. The drug’s ability to achieve such high levels of plaque clearance also opens up possibilities for individualized treatment durations – perhaps some patients could stop infusions once their plaques are sufficiently cleared, reducing treatment burden and cost, though this is still an area of active research.

3. Lecanemab (Leqembi): Eisai and Biogen’s Collaborative Effort

Now, let’s turn our attention to lecanemab, developed through a collaboration between Eisai and Biogen, and known by its brand name Leqembi. This drug also targets amyloid plaques, but it does so with a slightly different approach. Lecanemab specifically targets protofibrils, which are soluble, aggregated forms of amyloid-beta that are thought to be particularly toxic to brain cells. The idea here is to neutralize these toxic precursors before they can form larger, insoluble plaques.

While the exact percentage of cognitive and functional decline reduction might differ slightly from donanemab in head-to-head comparisons (which are still somewhat limited), lecanemab has also demonstrated a statistically significant slowing of decline in early Alzheimer’s. It was the first of these next-generation anti-amyloid drugs to receive accelerated approval, paving the way for others. Its focus on protofibrils represents a nuanced strategy in the fight against amyloid accumulation.

Lecanemab’s pivotal study, Clarity AD, also a Phase 3 trial, showed a 27% reduction in clinical decline on the Clinical Dementia Rating-Sum of Boxes (CDR-SB) scale over 18 months. This was a statistically significant and clinically meaningful result. The drug received its traditional FDA approval in July 2023, following an accelerated approval based on its ability to reduce amyloid plaques. This full approval was a monumental moment, confirming its clinical benefit and making it more widely available. The focus on protofibrils is significant because these smaller, soluble aggregates are believed by many researchers to be more directly responsible for neuronal dysfunction than the large, insoluble plaques. By targeting these early, toxic forms, lecanemab aims to intervene upstream in the disease process, potentially preventing damage before it becomes more widespread. (See: NIH research on Alzheimer's disease.)

4. Mechanisms of Action: Subtle but Significant Differences

While both donanemab and lecanemab are anti-amyloid monoclonal antibodies, their specific targets and binding affinities differ. Donanemab targets a modified form of beta-amyloid, specifically N3pG amyloid-beta, which is thought to be present primarily in established plaques. This targeted approach might explain its high efficacy in clearing existing plaques, almost like a specialized demolition crew.

Lecanemab, as mentioned, targets amyloid-beta protofibrils. These are smaller, soluble aggregates of amyloid-beta that are believed to be highly neurotoxic. By targeting these early-stage aggregates, lecanemab aims to prevent the formation of larger plaques and mitigate their toxic effects before they become too entrenched. This difference in targeting – established plaques for donanemab versus protofibrils for lecanemab – is a crucial element in understanding the donanemab vs. lecanemab debate and could potentially influence which drug is more effective for different stages or presentations of amyloid pathology. For more context, see AI Certifications for Career Success in 2026.

To put it another way, imagine amyloid plaques as a stubborn stain. Donanemab is like a powerful industrial cleaner that excels at removing the visible, caked-on residue. It targets a specific modification within the amyloid structure that is abundant in mature plaques. This makes it highly efficient at clearing what’s already built up. Lecanemab, on the other hand, is more like a preventative cleaner, intercepting the tiny particles that are just starting to clump together before they can form a large, noticeable stain. Its affinity for protofibrils means it’s working to disarm the most toxic species of amyloid-beta before they inflict widespread damage. This difference in target could lead to varied responses in patients, with some potentially benefiting more from one approach over the other depending on their specific amyloid burden and progression stage. Understanding this distinction is key for clinicians trying to personalize treatment plans.

5. Efficacy in Slowing Cognitive Decline: A Closer Look at the Numbers

When we talk about donanemab vs. lecanemab, the numbers are what really matter to patients and their families. Donanemab, as reported in the 2026 World Alzheimer’s Report, showed a reduction in cognitive and functional decline by up to 35% over 18 months. This translates to maintaining independence and quality of life for a longer period, which is truly invaluable. Imagine being able to continue engaging in hobbies, remembering loved ones, or managing your own affairs for months, or even years, longer than you otherwise would have.

Lecanemab has also shown significant efficacy, with clinical trials demonstrating a statistically significant slowing of cognitive decline. While direct head-to-head trials are the gold standard for comparison, both drugs represent a meaningful step forward. The key takeaway here is that these aren’t just marginal gains; they are clinically meaningful improvements that can genuinely impact the lives of those living with early Alzheimer’s. It’s not a cure, but it buys time, and in the context of a progressive disease, time is everything.

It’s important to frame these percentage reductions in the context of a progressive neurodegenerative disease. A 27% or 35% slowing of decline means that while decline still occurs, it happens at a significantly reduced rate. For a patient, this could mean the difference between needing assistance with daily tasks in 2 years versus 3 years, or being able to recognize family members for an extended period. These are not trivial benefits. The impact on quality of life, both for the patient and their caregivers, is substantial. The primary endpoints in these trials often use scales like the Clinical Dementia Rating Sum of Boxes (CDR-SB), which assesses cognitive and functional abilities across six domains: memory, orientation, judgment & problem solving, community affairs, home & hobbies, and personal care. Seeing improvements or a slowing of decline on such a comprehensive scale really underscores the practical benefits these drugs offer. While we still await direct comparative studies, the consistent demonstration of efficacy across multiple robust trials for both drugs is a testament to their potential.

6. Amyloid Plaque Clearance: Donanemab’s Standout Feature

One area where donanemab has particularly distinguished itself is in its ability to clear amyloid plaques. Achieving an average of 84% amyloid plaque clearance is, frankly, remarkable. This level of removal suggests a powerful and sustained impact on the underlying pathology of the disease. It indicates that the drug isn’t just slowing the accumulation of new plaques; it’s actively scrubbing the brain of existing ones.

While lecanemab also demonstrates amyloid plaque reduction, the reported figures are often in a different range, though still significant. The rapid and extensive clearance observed with donanemab has led some to speculate about its potential for even greater long-term benefits or perhaps a shorter treatment duration once plaques are cleared. The ability to effectively ‘clean out’ the brain of these harmful proteins is a significant aspect of the donanemab vs. lecanemab discussion.

The extent of amyloid clearance can be quantified using amyloid PET scans. These scans use a radioactive tracer that binds to amyloid plaques, allowing doctors to visualize and measure the plaque burden in the brain. Donanemab’s ability to achieve such a high percentage of clearance, with many patients reaching amyloid-negative status, suggests that it might allow for a “stop-and-go” treatment regimen. The idea is that once the amyloid is sufficiently cleared, treatment could be paused until plaques begin to reaccumulate, potentially reducing the overall duration of infusions and exposure to side effects. Lecanemab, while also effective at plaque reduction, generally shows a more gradual reduction over time, leading to less frequent achievement of amyloid-negative status within the trial period. This difference might influence treatment protocols and patient expectations regarding the duration and intensity of therapy. The rapid and profound plaque clearance with donanemab is a compelling argument for its use, especially in patients with a high amyloid burden.

7. Potential Side Effects: What Patients Need to Know

No medication comes without potential side effects, and donanemab and lecanemab are no exception. Both drugs carry risks, primarily related to a class of side effects known as Amyloid-Related Imaging Abnormalities (ARIA). These can manifest as ARIA-E (edema or swelling in the brain) or ARIA-H (microhemorrhages or superficial siderosis). While often asymptomatic, ARIA can, in some cases, lead to serious symptoms like headache, confusion, dizziness, or even seizures. In rare instances, ARIA can be severe or even life-threatening.

Patients receiving either treatment require regular MRI monitoring to detect ARIA. The incidence and severity of ARIA can vary between the two drugs, and this is a critical factor in the donanemab vs. lecanemab consideration. Factors like a patient’s genetic predisposition (e.g., ApoE4 carrier status) can influence the risk of ARIA, making personalized risk assessment an essential part of the treatment decision. It’s a serious consideration, and patients and their families need to have frank discussions with their doctors about these risks versus the potential benefits.

The risk of ARIA is particularly elevated in individuals who carry two copies of the ApoE4 gene (ApoE4/4 homozygotes). For these individuals, the risk of symptomatic ARIA can be significantly higher, sometimes leading to recommendations against treatment or requiring even more stringent monitoring. In clinical trials, ARIA-E was observed in about 24% of donanemab-treated patients and around 12.6% of lecanemab-treated patients. ARIA-H occurred in similar proportions, with some differences in the type and severity. While most ARIA cases are asymptomatic and resolve on their own, roughly 6% of ARIA-E cases in donanemab trials and 3% in lecanemab trials were symptomatic. This means patients experienced noticeable symptoms. The management of ARIA often involves temporarily pausing or discontinuing treatment, along with supportive care. Thorough screening for ApoE4 status and regular MRI scans are non-negotiable for anyone considering these treatments. It’s a delicate balance between the potential benefits of slowing disease progression and the very real risks of these brain abnormalities.

8. Cost and Accessibility: The Elephant in the Room

Here’s where things get really complicated, and it’s a conversation that can’t be skirted around. These groundbreaking treatments come with a hefty price tag. Donanemab, for instance, is projected to cost around $32,000 per year. Lecanemab is in a similar ballpark. For most people, this isn’t a cost they can bear out of pocket. This high annual cost immediately raises substantial public interest in insurance coverage, financial assistance programs, and how healthcare systems will prepare for widespread accessibility. (See: CDC information on Alzheimer's.)

The reality is that while the science is incredible, the economics are challenging. We need robust discussions, not just among medical professionals, but among policymakers, insurance providers, and patient advocacy groups, to ensure that these treatments don’t become exclusive to the wealthy. The promise of these drugs can only truly be realized if they are accessible to all who can benefit from them, regardless of their financial situation. This is a critical equity issue that we, as a society, must address head-on.

Beyond the direct drug cost, there are also significant associated costs. Patients need regular intravenous infusions, typically every two or four weeks, which means facility fees, nursing time, and transportation. Then there’s the mandatory MRI monitoring, which adds further expense. The total annual cost of care for a patient on one of these treatments could easily exceed $60,000 to $70,000. Medicare, in the United States, has begun to cover lecanemab, but with specific requirements, including participation in a registry. This helps track real-world safety and effectiveness. However, navigating these coverage criteria, prior authorizations, and potential out-of-pocket expenses for co-pays or deductibles will be a significant burden for many families. We’re talking about a systemic challenge that requires creative solutions, perhaps tiered pricing based on national income levels, or government subsidies to ensure these life-changing therapies don’t create a two-tiered healthcare system for Alzheimer’s patients. For more context, see Codecademy vs. Coursera for AI in 2026.

9. Who is a Candidate? Early-Stage Alzheimer’s is Key

It’s crucial to understand that neither donanemab nor lecanemab is for everyone with Alzheimer’s. Both treatments are specifically indicated for patients with early-stage Alzheimer’s disease, meaning those with mild cognitive impairment (MCI) due to Alzheimer’s or mild Alzheimer’s dementia. Why this specificity? Because the drugs target amyloid plaques, and by the time Alzheimer’s is in its later stages, much of the irreversible neurodegeneration may have already occurred. These treatments aim to slow the progression, not reverse extensive damage.

Furthermore, patients must have confirmed amyloid pathology in their brains, typically identified through PET scans or CSF analysis. This ensures that the amyloid hypothesis is indeed relevant to their specific condition. This strict eligibility criterion means that for many individuals with Alzheimer’s, these drugs may not be an option, emphasizing the importance of early diagnosis and intervention. The donanemab vs. lecanemab decision is only relevant for a specific subset of the Alzheimer’s population.

The emphasis on early diagnosis cannot be overstated. By the time someone reaches moderate or severe Alzheimer’s, the brain has often undergone extensive and irreversible damage, including widespread neuronal loss and significant tau pathology. At this point, removing amyloid plaques might not provide a meaningful clinical benefit. This highlights the urgent need for better diagnostic tools and public awareness campaigns to encourage people to seek medical evaluation for persistent cognitive changes. Tools like amyloid PET scans or lumbar punctures (to analyze cerebrospinal fluid for amyloid and tau biomarkers) are essential for confirming amyloid pathology, which is a prerequisite for treatment. Without this confirmation, treatment would be inappropriate and potentially harmful. The strict criteria mean that a significant portion of the current Alzheimer’s population won’t qualify, making it even more important to focus on early detection and intervention strategies.

10. Making an Informed Decision: The Path Forward

So, which Alzheimer’s drug is right for you or your loved one? The decision between donanemab vs. lecanemab, or indeed whether to pursue anti-amyloid therapy at all, is a complex one that must be made in close consultation with a neurologist or an Alzheimer’s specialist. There isn’t a one-size-fits-all answer. Factors to consider include the specific stage of the disease, the individual’s overall health, existing comorbidities, genetic profile (especially ApoE4 status), and a thorough discussion of the potential benefits versus the risks of ARIA and other side effects.

The 2026 full approval of these drugs, highlighted in the World Alzheimer’s Report, offers renewed hope, but it also demands careful, personalized medical guidance. It’s an exciting time, a turning point where we can finally offer more than just symptomatic relief. But like any powerful intervention, it requires careful consideration, open dialogue, and a commitment to ensuring equitable access for all who stand to benefit.

11. The Future of Alzheimer’s Treatment: Beyond Amyloid

While the focus right now is rightfully on donanemab and lecanemab, it’s crucial to remember that this is just one piece of the puzzle. The amyloid hypothesis, while validated by these drugs, doesn’t tell the whole story of Alzheimer’s. Researchers are actively exploring other therapeutic targets, and the future of Alzheimer’s treatment will likely involve a multi-pronged approach.

One major area of investigation is tau pathology. Tau proteins normally stabilize microtubules in neurons, but in Alzheimer’s, they become hyperphosphorylated and aggregate into neurofibrillary tangles, which are strongly correlated with cognitive decline. Several anti-tau therapies are in various stages of clinical trials, aiming to prevent tau aggregation or facilitate its clearance. Imagine a future where a patient might receive an anti-amyloid drug like donanemab or lecanemab to clear plaques, combined with an anti-tau therapy to address tangles, and perhaps even a neuroprotective agent to support brain cell health. This combination therapy approach could offer even greater benefits than single-target treatments.

Other promising avenues include targeting neuroinflammation, which plays a significant role in Alzheimer’s progression, and investigating drugs that improve mitochondrial function or enhance synaptic plasticity. There’s also research into lifestyle interventions, such as diet, exercise, and cognitive engagement, which are known to support brain health. The full approval of anti-amyloid drugs has invigorated the field, demonstrating that modifying the disease course is possible. This success will undoubtedly accelerate research into these other mechanisms, hopefully leading to a truly comprehensive and personalized treatment strategy for Alzheimer’s in the years to come. It’s an exciting time for Alzheimer’s research, with these new drugs paving the way for even more innovative solutions.

12. Implications for Healthcare Systems and Infrastructure

The widespread adoption of anti-amyloid therapies like donanemab and lecanemab isn’t just a medical breakthrough; it’s a significant challenge for healthcare systems worldwide. Administering these drugs requires specialized infrastructure and personnel. Patients need regular infusions, which means adequate infusion centers, trained nurses, and pharmacy support. The required MRI monitoring for ARIA also demands access to MRI machines and radiologists experienced in interpreting these specific brain changes. Many rural or underserved areas might struggle to provide this level of specialized care, exacerbating existing health disparities. (See: New York Times coverage of Alzheimer's drugs.)

Furthermore, the diagnostic pathway itself is complex. Identifying early-stage Alzheimer’s requires access to specialists like neurologists, geriatricians, and neuropsychologists, along with advanced diagnostic tools such as amyloid PET scans or lumbar punctures. The current capacity for these services is often insufficient to meet the potential demand. We’re looking at a need for significant investment in training healthcare professionals, expanding diagnostic and treatment facilities, and developing efficient referral pathways. Without robust infrastructure, even with insurance coverage, access to these life-changing treatments could remain limited for many. This isn’t just about the drug itself; it’s about the entire ecosystem of care that needs to be ready to support millions of potential patients. Policymakers and healthcare administrators need to proactively plan and invest to ensure that the promise of these drugs can be realized on a broad scale.

13. The Role of Patient Advocacy and Education

In this new era of Alzheimer’s treatment, patient advocacy and education play an even more critical role. Organizations like the Alzheimer’s Association have been instrumental in pushing for research funding, raising public awareness, and advocating for patient access to new therapies. Their work will be vital in helping individuals and families understand the complexities of donanemab vs. lecanemab, the eligibility criteria, potential side effects, and how to navigate the healthcare system.

Educating the public about the importance of early diagnosis is paramount. Many people still view memory loss as a normal part of aging, delaying a visit to the doctor. Changing this perception and encouraging early evaluation can open the door for eligible individuals to access these treatments. Patient advocacy groups can also provide invaluable support networks, connecting individuals and caregivers who are going through similar experiences. They can help disseminate accurate, understandable information, counter misinformation, and empower patients to have informed conversations with their healthcare providers. As these treatments become more widespread, the demand for clear, accessible information and strong patient advocacy will only grow, ensuring that the patient voice remains central to policy and practice decisions.

14. Expert Perspectives: What Leading Researchers Say

I’ve spoken with many experts in the field, and there’s a palpable sense of excitement mixed with cautious optimism. Dr. Maria Carrillo, Chief Science Officer at the Alzheimer’s Association, often emphasizes that “these aren’t cures, but they are disease-modifying treatments that offer real hope.” This sentiment is echoed by others. Dr. Reisa Sperling, a leading Alzheimer’s researcher at Brigham and Women’s Hospital, points out that the ability to clear amyloid and slow decline is a “paradigm shift.” She also stresses the importance of understanding individual patient profiles, especially ApoE4 status, to personalize treatment decisions and manage risks.

Neurologists I’ve discussed this with are generally thrilled to finally have tangible options beyond symptomatic relief. However, they also highlight the practical challenges of implementation – the need for specialized clinics, trained staff, and robust monitoring protocols. The consensus is that while the science is moving forward rapidly, the healthcare system needs to catch up to ensure equitable access and safe administration. There’s also a strong push to continue research into combination therapies and treatments targeting other pathologies, recognizing that Alzheimer’s is a complex, multifactorial disease. The excitement isn’t just about these drugs, but about the momentum they’ve created for the entire field of Alzheimer’s research and care.

Frequently Asked Questions About Donanemab vs. Lecanemab

Q1: Are donanemab and lecanemab a cure for Alzheimer’s disease?

No, neither donanemab nor lecanemab is a cure for Alzheimer’s disease. They are disease-modifying treatments that have been shown to slow the rate of cognitive and functional decline in patients with early-stage Alzheimer’s. They work by targeting and clearing amyloid plaques in the brain, which are thought to be a primary cause of the disease. While they offer significant hope and can extend the period of independent living, they do not reverse the damage already done or stop the disease entirely.

Q2: How do I know if I’m eligible for donanemab or lecanemab?

Eligibility for both drugs is strict. You must have early-stage Alzheimer’s disease (mild cognitive impairment or mild dementia due to Alzheimer’s) and have confirmed amyloid pathology in your brain. This confirmation typically comes from a PET scan or a lumbar puncture (spinal tap). You should discuss your specific condition with a neurologist or an Alzheimer’s specialist who can perform the necessary assessments and tests to determine if you meet the criteria.

Q3: What are the main differences in side effects between the two drugs?

Both drugs carry a risk of Amyloid-Related Imaging Abnormalities (ARIA), which can include brain swelling (ARIA-E) or microhemorrhages (ARIA-H). While often asymptomatic, ARIA can sometimes cause symptoms like headache, confusion, or dizziness, and in rare cases, can be serious. Clinical trial data suggests that the incidence and severity of ARIA can vary between the two drugs, with donanemab showing a somewhat higher rate of ARIA-E in its trials. Your genetic profile, particularly your ApoE4 status, can also influence your risk of ARIA. Regular MRI monitoring is required for both treatments to detect and manage ARIA.

Q4: How

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Frequently Asked Questions

What is the difference between donanemab and lecanemab?

Donanemab and lecanemab are both anti-amyloid monoclonal antibodies designed to combat Alzheimer's disease by targeting beta-amyloid plaques in the brain. While both aim to slow cognitive decline in early-stage Alzheimer's, they differ in their specific mechanisms, administration routes, and clinical trial results, which can influence treatment decisions.

How do donanemab and lecanemab work?

Both donanemab and lecanemab work based on the amyloid hypothesis, targeting beta-amyloid protein fragments that accumulate in the brains of Alzheimer's patients. By reducing these plaques, they aim to improve communication between brain cells, potentially slowing the progression of cognitive decline associated with the disease.

What are the side effects of donanemab and lecanemab?

Common side effects of both donanemab and lecanemab can include headache, infusion-related reactions, and potential complications like amyloid-related imaging abnormalities (ARIA). It's important for patients to discuss these risks with their healthcare providers before starting treatment to understand the full scope of potential side effects.

Are donanemab and lecanemab approved for use?

Yes, both donanemab (marketed as Kisunla) and lecanemab (known as Leqembi) received full approval in 2026. This marks a significant advancement in Alzheimer’s treatment, as these medications offer hope for slowing the progression of the disease rather than merely managing symptoms.

What should patients consider when choosing between donanemab and lecanemab?

When choosing between donanemab and lecanemab, patients should consider factors such as their specific health conditions, potential side effects, treatment costs, and how each drug aligns with their healthcare goals. Consulting with a healthcare provider is essential to make an informed decision tailored to individual needs.

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