Anti-Amyloid Therapies for Alzheimer’s Highlighted at International Conference

For years, Alzheimer’s disease news mostly sounded the same: lots of hopeful lab data, not much that changed life in the clinic. That tone shifted dramatically at recent international Alzheimer’s conferences, where anti-amyloid therapiesespecially monoclonal antibodies like lecanemab (Leqembi) and donanemab (Kisunla)took center stage. Long-term results, real-world data, and updated safety findings made it clear that we’ve officially entered the era of disease-modifying treatment, even if that era is messy, expensive, and far from perfect.

In this in-depth guide, we’ll unpack what anti-amyloid therapies are, why they generated so much buzz at the latest international meetings, what the benefits and risks look like in real life, and how patients and families are navigating this new landscape.

What Are Anti-Amyloid Therapies, Exactly?

Alzheimer’s disease is strongly associated with the buildup of sticky protein clumps called amyloid-beta plaques in the brain. For decades, researchers have suspected that these plaques play a central role in damaging brain cellsa concept known as the amyloid hypothesis.

Anti-amyloid therapies are drugs designed to clear or reduce these plaques. The most talked-about treatments in this class are monoclonal antibodieslab-made antibodies that latch onto amyloid and flag it for removal by the immune system:

• Aducanumab (Aduhelm) – the first anti-amyloid antibody to get U.S. approval for early Alzheimer’s, though its controversial data and limited coverage severely restricted its use.
• Lecanemab (Leqembi) – the first fully approved disease-modifying therapy in the U.S. for early Alzheimer’s, now backed by extensive long-term data.
• Donanemab (Kisunla) – another antibody recently approved in the U.S. for early symptomatic Alzheimer’s, with evidence that it can be stopped once amyloid is cleared.

These drugs are very different from older medications like donepezil or memantine, which help symptoms but don’t change the underlying disease process. Anti-amyloid therapies aim to actually slow disease progression, not just mask it.

The Stars of the Show: Lecanemab and Donanemab

Lecanemab (Leqembi): Slowing Decline and Staying in the Spotlight

Lecanemab targets amyloid “protofibrils,” intermediate forms of amyloid that contribute to plaque formation. In the pivotal phase 3 Clarity AD trial, people with early Alzheimer’s receiving lecanemab experienced about a 27% slower decline on a key cognitive and functional scale over 18 months compared with placebo. That difference may sound modest on paper, but for families, it can translate into extra months of being able to manage finances, recognize loved ones, or live more independently.

At recent international conferences, lecanemab data went from “exciting” to “seriously long-term.” New analyses presented at the Alzheimer’s Association International Conference (AAIC) and related meetings showed that patients followed for up to four years continued to experience slower cognitive decline than expected, with no new major safety concerns beyond what was seen early in treatment.

Highlights from these presentations included:

• Sustained slowing of declineroughly 34% slower cognitive worsening at four years compared with modeled untreated patients.
• High rates of amyloid plaque clearance on PET imaging and the ability to maintain lower amyloid levels over time.
• Development of subcutaneous (under-the-skin) formulations that could someday move treatment out of infusion centers and closer to home.

In other words: lecanemab hasn’t turned back the clock on Alzheimer’s, but it consistently nudges that clock to tick a little more slowly.

Donanemab (Kisunla): Clearing Fast, Then Stopping

Donanemab, marketed as Kisunla, takes a slightly different approach. It targets a specific, modified form of amyloid-beta found in plaques and appears to clear those plaques relatively quickly. In the phase 3 TRAILBLAZER-ALZ 2 trial, donanemab significantly slowed cognitive and functional decline in people with early symptomatic Alzheimer’s and amyloid plus tau pathology.

One particularly intriguing feature: many participants were able to stop treatment once their amyloid plaques were cleared below a certain threshold, rather than staying on therapy indefinitely. Long-term extension data presented in 2025 showed that patients who started donanemab earlier and achieved robust amyloid clearance enjoyed sustained benefits over three years, with continued slower progression and high rates of plaque removal.

That “treat until amyloid is gone” model has big implications for cost, logistics, and patient experiencethough doctors are still figuring out exactly who can stop, when, and how closely they should be monitored afterward.

Aducanumab (Aduhelm): The Cautionary Trailblazer

It’s impossible to talk about anti-amyloid antibodies without mentioning aducanumab. Aducanumab was the first of these drugs to win accelerated approval in the U.S., but conflicting trial data, safety worries, and payer pushback severely limited its real-world use. Many experts now view aducanumab as a “proof-of-concept” story: it helped open the regulatory door but also showed how controversial and complicated that path could be.

The lessons learned from aducanumababout trial design, meaningful outcomes, and safety communicationheavily shaped how lecanemab and donanemab were studied and rolled out.

What International Conferences Are Revealing Now

At recent international meetings like AAIC 2024 and 2025 and the International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD), anti-amyloid therapies took top billing again and again. The focus has shifted from “Do these drugs work at all?” to more practical, nuanced questions:

• How do they perform over several years in real-world populations, not just pristine clinical trial volunteers?
• Which patients benefit most, and at what point in the disease course?
• How do we minimize and manage side effects like amyloid-related imaging abnormalities (ARIA)?
• What does it take for health systems to actually deliver these therapies at scale?

Conference sessions highlighted multi-year open-label extension data, real-world case series, and subgroup analyses that help refine patient selection and monitoring strategies. Presentations also showcased work on subcutaneous dosing, combination approaches, and next-generation antibodies, as well as head-to-head comparisons of trial data for lecanemab and donanemab.

The big-picture takeaway from these meetings? Anti-amyloid therapy is no longer theoreticalit’s something clinics are implementing, tweaking, and stress-testing in real time.

What “Slowing Cognitive Decline” Really Means

A lot of the numbers tossed around at conferences27% slower decline here, 34% slower therecan feel abstract. So what does this look like in real life?

In the Clarity AD trial, the 27% slowing of decline with lecanemab was measured on a composite scale that blends cognition (like memory and problem-solving) with daily function (like managing finances or handling chores). Think of it like this: if someone on placebo loses 10 “points” of ability over 18 months, someone on treatment might lose around 7 to 8 points instead. It’s not stopping the disease, but it’s pushing the curve downward and stretching out the more independent years.

Similar patterns show up in donanemab data. Patients receiving the drug have fewer amyloid plaques, slower clinical decline, and a somewhat delayed need for higher levels of carenot a miracle cure, but a meaningful shift for people who are trying to preserve quality of life for as long as possible.

It’s helpful to think of these drugs as hitting the “slow motion” button rather than flipping the story from tragedy to fairy tale.

Risks, ARIA, and the Need for Careful Monitoring

Anti-amyloid therapies are powerful, and powerful tools almost always come with trade-offs. The main safety concern that dominated early discussionsand still gets prime airtime at conferencesis amyloid-related imaging abnormalities (ARIA).

ARIA mostly comes in two flavors:

• ARIA-E – brain swelling (edema or effusion) often seen on MRI; sometimes causes headaches, confusion, or visual changes, though many cases are asymptomatic.
• ARIA-H – small areas of bleeding in the brain (microhemorrhages) or superficial siderosis.

In trials of lecanemab, ARIA-E occurred in around 12–13% of treated participants, with higher rates in those who carry the APOE ε4 genetic variant associated with higher Alzheimer’s risk. Donanemab shows similar safety concerns, particularly in people with certain risk profiles.

That’s why appropriate-use guidelines and conference sessions emphasize:

• Screening for amyloid and, in some cases, tau pathology before treatment.
• Baseline and regular follow-up MRIs to catch ARIA early.
• Cautious dosing and close monitoring in people with multiple microbleeds or high vascular risk.
• Clear communication so patients and families understand both benefits and potential risks.

The bottom line is that anti-amyloid therapy isn’t a “set it and forget it” infusionit’s a structured program that demands specialist oversight, imaging resources, and informed decision-making.

Practical Realities: Cost, Access, and Health-System Growing Pains

If science conferences are where anti-amyloid therapies shine, health systems are where reality sets in. These drugs are expensive, require frequent infusions or injections, and demand access to PET imaging or blood biomarkers plus repeated MRIs.

International discussions have highlighted:

• Coverage differences between countries and even within regions, with some health authorities questioning whether the modest clinical benefit justifies the cost and safety risks.
• Equity concerns, since people who live far from large medical centers or lack specialist access may be effectively locked out of treatment.
• Infrastructure challenges around infusion capacity, MRI scheduling, and training multidisciplinary teams to handle workups, counseling, and follow-up.

These issues are increasingly part of the “hot topics” track at major conferences. The science might say, “Yes, this works,” but clinicians and policymakers still have to answer, “Can we actually deliver it fairly?”

Where Do Anti-Amyloid Therapies Fit in Today’s Alzheimer’s Care?

With all this buzz, it’s natural for families to wonder: Should we be asking about these drugs? The answer is a very qualified “maybe.”

Right now, anti-amyloid antibodies are generally used for:

• People with early-stage Alzheimer’smild cognitive impairment or mild dementia due to Alzheimer’s.
• Patients with confirmed amyloid pathology, usually by PET scan or specialized blood and CSF tests.
• Individuals who can safely undergo repeated MRIs and are not at high risk of serious ARIA.

Even for those who qualify, anti-amyloid therapy is just one piece of a much bigger care puzzle that still includes:

• Symptomatic medications (when appropriate).
• Management of sleep, mood, blood pressure, and other health conditions.
• Structured routines, cognitive engagement, and social support.
• Caregiver training and community resources.

If you or a loved one is considering these treatments, the best first step is a frank conversation with a dementia specialistideally someone who is familiar with lecanemab and donanemab, keeps up with conference data, and can walk you through the practical details and trade-offs in your specific situation.

Experiences from the Front Lines: How Anti-Amyloid Therapies Feel in Real Life

Conference slides and p-values are important, but they don’t quite capture what anti-amyloid therapy means in everyday life. Many of the most powerful “data points” actually come from layered, real-world experiences described by patients, families, and cliniciansoften shared in panels, Q&A sessions, and hallway conversations.

A Caregiver’s View: Buying Time, Not Miracles

Picture a daughter in her 50s sitting in an auditorium at an international Alzheimer’s conference. Her mom, recently diagnosed with early Alzheimer’s, started lecanemab about 10 months ago. Before treatment, every month felt like a small but noticeable step downmore repeated questions, more lost items, more appointments she didn’t remember.

Since starting therapy, the daughter wouldn’t say her mother is “back to normal.” But the slide has felt less steep. Her mom still remembers the names of her grandchildren and can follow the plot of a TV show a little better than the daughter expected. There are still rough days, but they’re not accelerating in the way she feared. That’s the kind of “slowed decline” many families describenot a rewind button, but a subtle smoothing of the trajectory.

At the conference, the daughter listens to talks about four-year data and long-term extension trials and quietly thinks, “If we can stretch the good years just a bit more, that’s worth a lot.”

A Neurologist’s Experience: Hope with a Side of Complexity

For clinicians, anti-amyloid therapies have brought a new emotional mix: excitement, responsibility, and a healthy dose of anxiety. One memory clinic neurologist might describe how their practice shifted from simply diagnosing and counseling to building an entire anti-amyloid “pipeline”: coordinating amyloid testing, arranging MRI slots, counseling about ARIA, and fielding phone calls from worried families after every headache or stumble.

At a recent international meeting, this neurologist shares a story during a panel: a patient on lecanemab developed ARIA-Ebrain swelling visible on MRIafter a few infusions. The patient had mild confusion and headache, so the team paused treatment, monitored closely, and watched the swelling resolve. The experience was nerve-racking but ultimately manageable. It reinforced what conference experts keep saying: these therapies can be used safely, but only with robust protocols, quick access to imaging, and clear communication about warning signs.

The neurologist adds a candid note: “It’s a lot of work, but it’s also the first time I’ve been able to tell patients, ‘We have something that may actually change the course of the disease, not just manage symptoms.’ That’s a big emotional shift for everyone in the room.”

A Family in a Donanemab Trial: The Power of “Good Enough”

Another commonly shared type of story comes from families involved in donanemab studies. One spouse explains that when their partner enrolled in a trial, they weren’t expecting miraclesthey just hoped to slow things down. Over the course of the study, they still saw memory slips and occasional confusion, but the rate of change felt slower than friends’ experiences with Alzheimer’s years prior.

When MRI showed that amyloid plaques were largely cleared, the team stopped infusions as per the trial protocol. The spouse describes mixed feelings: relief at fewer hospital visits, but also anxiety about whether stopping would cause the disease to “speed up again.” Months later, they’re still doing reasonably wellneeding reminders, yes, but still engaged in hobbies and family routines. For them, the value of therapy lies not in dramatic improvement but in maintaining familiar routines for longer than they expected.

Health-System Voices: Stretching the System to Meet the Moment

At the system level, administrators and clinic leaders share their own war stories: scrambling to add infusion chairs, negotiating with insurers, and trying to ensure that people in rural or underserved communities aren’t left behind. At one conference roundtable, a healthcare leader notes that adopting anti-amyloid therapies has forced them to rethink everything from referral pathways to MRI scheduling.

They describe piloting “Alzheimer’s infusion days,” where neurologists, nurses, pharmacists, and social workers all coordinate to streamline visits and provide education. It’s not glamorous, but it’s the kind of operational detail that makes the difference between a therapy existing on paper and being available to real people.

Put together, these experiencespatients gaining a slower slide, families recalibrating expectations, clinicians balancing hope and caution, and health systems stretching to keep upare exactly what international conferences are bringing into focus. Anti-amyloid therapies are not a sci-fi cure, but they’re reshaping the Alzheimer’s story in small, steady, and increasingly measurable ways.

Conclusion: A New Chapter, Not the Final Page

Anti-amyloid therapies like lecanemab and donanemab have moved from bold hypothesis to real-world practice, and recent international conferences have made that evolution impossible to ignore. We now have multi-year data showing sustained slowing of cognitive and functional decline, detailed guidance on how to use these drugs more safely, and growing experience from clinics around the world.

At the same time, the story is far from complete. Access remains uneven, safety monitoring is complex, and the benefitswhile meaningfulare not transformative for everyone. Future conferences will likely highlight combination therapies, tau-targeting drugs, and better biomarkers to match the right treatment to the right person at the right time.

For now, anti-amyloid therapies represent a new chapter in Alzheimer’s care: not a cure, but a genuine shift from “nothing can change the course of this disease” to “we can slow it down.” For many patients and families, that shift is worth talking aboutand, for some, worth pursuingtogether with an experienced clinical team.