For most of the last century, an Alzheimer's diagnosis came with the same answer: there's nothing that can change how this disease unfolds. That's no longer true. Since 2023, two medicines have been approved that clear amyloid plaques from the brain and slow decline in people with early symptoms. Since 2025, a blood test can help confirm the diagnosis without needing a brain scan. The gains are real, but modest, and they come with a catch: they only work early on, and most people are still diagnosed too late.
More than 7 million Americans live with Alzheimer's today, and that number is expected to grow to nearly 13 million by 2050. This article covers what treatment looks like today, what a very public failure in late 2025 taught the field, what researchers are testing right now, and why the most important trials now enroll people who feel perfectly fine.
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What Alzheimer's treatment includes today
The older medicines. Donepezil (Aricept), rivastigmine, galantamine, and memantine have all been around for 20 years or more. They ease symptoms for a while by boosting chemical signals between brain cells, but they don't slow the disease itself. They're still standard because they genuinely help, and because for decades they were all there was.
The amyloid clearing antibodies. Lecanemab (Leqembi) received full FDA approval in July 2023. In its 18 month trial, it slowed decline on a combined thinking and daily function scale by 27 percent compared with placebo. Donanemab (Kisunla) followed in July 2024, slowing decline by 35 percent in its trial. Both are given as infusions every two to four weeks, both require confirmed amyloid before starting, and both need regular MRI scans, because in a small number of people they can cause brain swelling or small bleeds, called ARIA. In 2025 a version of lecanemab given as a weekly injection under the skin was also approved for maintenance, which some people can take at home. These medicines slow the disease, they don't stop or reverse it, and right now they're only approved for mild cognitive impairment and mild dementia.
The blood test. In May 2025 the FDA cleared the first blood test to help diagnose Alzheimer's, which measures the ratio of pTau217 to amyloid. It's approved for people 55 and older who already have symptoms. It picks up the same plaques that used to require a PET scan or a spinal tap. It's not a standalone diagnosis on its own, and it's not meant to screen people without symptoms, but it removes a big barrier to getting treated in time.
Symptom treatments. Agitation, psychosis, trouble sleeping, and depression are often what wear families down the most. Brexpiprazole was approved for agitation in Alzheimer's in 2023, and several trials for psychosis are currently underway.
What the field learned in November 2025
Semaglutide, the diabetes and weight loss medicine sold as Ozempic and Wegovy, had shown some early signs of protecting the brain in earlier studies, and hopes were high. Novo Nordisk ran two large trials, EVOKE and EVOKE+, in more than 3,800 people with early Alzheimer's, over two years. On November 24, 2025, the company announced the result: no real difference from placebo in thinking, daily function, or how quickly people moved from mild cognitive impairment to dementia, even though some biomarkers did move in the right direction. The full data, shown in March 2026, confirmed it. It was a disappointment, and also a good reminder of why trials exist in the first place: biomarkers improving isn't the same thing as people actually getting better.
What researchers are studying now
Prevention: treating people with no symptoms. The biggest idea in the field right now is that clearing amyloid works best before real damage happens. On our platform, a study of a potential disease changing treatment in people at risk and a second at risk study enroll people with normal memory who carry the rare gene mutation that causes early onset, inherited Alzheimer's, and ask whether treating them now can delay dementia by years. A tau vaccine study in preclinical Alzheimer's takes that same early approach, but against the other protein involved, tau.
A better antibody. Roche's trontinemab uses a "brain shuttle" to carry the antibody across the blood brain barrier more efficiently. In early trials, 91 percent of people on the higher dose had no detectable amyloid left after 28 weeks, and brain swelling showed up in fewer than 5 percent of people, much lower than with the antibodies already approved. Whether that actually leads to slower decline is exactly what the Phase 3 TRONTIER study, together with a companion trial, is now testing in people with early symptoms. Results aren't expected until around 2028. AbbVie is testing ABBV-1758, given as a shot under the skin or through an IV, in that same group of people.
Beyond amyloid. A study repurposing siponimod, a drug normally used for multiple sclerosis, is testing an anti inflammatory approach instead. A trial of gamma frequency light and sound stimulation is testing whether specific light and sound patterns can affect the disease with no drug involved at all. And an ExAblate focused ultrasound study is testing whether briefly opening the blood brain barrier can help clear plaques out.
The symptoms families struggle with. KarXT is being tested for psychosis in Alzheimer's, and so is ACP-204. Hallucinations and delusions affect a large share of people with moderate stage disease, and there aren't many safe treatments for them yet.
Why Alzheimer's research takes time
The slow disease problem. Alzheimer's develops over decades, and any change over 18 months is subtle. Proving a drug actually slows it down takes more than a thousand people, frequent brain scans, and careful cognitive testing, and that's just the minimum, a year and a half. Prevention trials take even longer, because they have to wait for dementia that might not show up for years.
The too late problem. The approved drugs only work in that early window, but most people get diagnosed after it's already passed. Finding a faster, cheaper way to diagnose people is just as much a research problem as a clinical one, and the 2025 blood test was the first big step toward that.
The biomarker trap. A drug can clear amyloid impressively, or shift blood markers in the right direction, and still not help people actually think better. Semaglutide moved the biomarkers and still failed. Earlier amyloid drugs, like bapineuzumab and aducanumab, ran into the same problem. Regulators and researchers now insist on seeing real improvement in thinking and daily function, not just better numbers on a test, which is the right standard, just a slow one.
The representation problem. Older Black Americans are about twice as likely, and older Hispanic Americans about one and a half times as likely, to develop Alzheimer's as older white Americans, yet both groups made up a small share of the trials that got today's drugs approved, especially Black participants, who were only around 2 to 3 percent in both major trials. Whether these drugs work equally well for everyone is still an open question, and several current studies name diverse enrollment as a specific goal. Here's why diversity in clinical trials matters so much.
Common myths about Alzheimer's
"Alzheimer's is just old age."
No, it's not. Most people over 85 don't actually have it, about a third do, which means two out of three don't. It's a specific disease with specific brain changes that start decades before any symptoms show up, and age is a risk factor, not the cause.
"If a parent had it, I will get it."
Usually not. There's a rare, early onset form that's strongly inherited, but most Alzheimer's is the late onset kind, where genes raise your risk without deciding the outcome. Most children of people with Alzheimer's never actually develop it.
"There is nothing you can do."
That's outdated. Two medicines can slow early disease, and research suggests that controlling blood pressure, staying active, treating hearing loss, and managing diabetes may lower your risk. Prevention trials are now testing whether even more is possible.
"A blood test can tell if I will get Alzheimer's."
Not yet, and not for people without symptoms. The test that's been cleared is for people 55 and older who already have memory concerns, and results still need to be looked at alongside a full evaluation. Prevention trials use similar tests to find people who qualify, which right now is really the main way to learn your amyloid status if you don't have symptoms.
The stages of Alzheimer's, and what care usually looks like
Doctors describe a preclinical stage first (amyloid is present, memory is still normal, this can last 15 to 20 years), then mild cognitive impairment, then mild, moderate, and severe dementia. Typical care: at the MCI and mild dementia stages, the conversation now includes testing for amyloid and, if it's found, the option of an amyloid clearing antibody alongside the older symptom medicines. At moderate stages, care shifts toward safety, routine, and managing agitation, sleep, and mood. At severe stages, comfort and support for caregivers become the main focus. This describes usual practice, not a recommendation, your family's plan belongs to you and the doctor.
For trials, the stage is usually right there in the name. Titles say "preclinical," "early symptomatic," or "mild to moderate," and drug trials often add "amyloid positive." Knowing the stage and whether amyloid has been confirmed is enough to filter through studies in minutes.
How to find an Alzheimer's clinical trial
AllClinicalTrials.com lists Alzheimer's studies recruiting across the US, everything from Phase 3 antibody trials to prevention studies, symptom trials, and biomarker research. Two examples recruiting right now: the Phase 3 TRONTIER study of trontinemab for people with early symptomatic Alzheimer's, and a prevention study for people who carry the rare gene mutation that causes inherited early onset Alzheimer's but haven't developed symptoms yet.
The application takes about 5 minutes and can be filled out by a family member. You'll answer questions about the diagnosis, any amyloid test results, and current medicines, and if a study near you looks like a match, the research team reaches out to you. Nothing is decided until you go through informed consent, which in Alzheimer's studies always involves a study partner too, and you can stop taking part at any point. Three things to have ready: the current diagnosis or stage, any amyloid results, and the name of a study partner who can come to visits with you.
Common questions
What is the newest treatment for Alzheimer's? Donanemab (Kisunla), approved in July 2024, is the most recent amyloid clearing drug, after lecanemab (Leqembi), which came in 2023. A version of lecanemab you inject under the skin was approved in 2025, and the first blood test to help with diagnosis was cleared in May 2025. Trontinemab is the drug everyone in the field is watching right now, in Phase 3 testing.
Is there a cure for Alzheimer's? No. The approved antibodies slow early disease by roughly a quarter to a third, but they don't stop it or reverse it. Prevention trials are testing whether treating people before symptoms even start could do more. No drug has ever reversed Alzheimer's in people.
How is Alzheimer's diagnosed? With memory and thinking tests, a medical history, brain imaging, and confirming amyloid through a blood test, a PET scan, or a spinal fluid test. Since 2025, the blood test can replace the scan in a lot of cases. A doctor puts all of this together, no single test can diagnose Alzheimer's on its own.
Do Alzheimer's trials use a placebo? Yes, in most drug trials, because there's no other way to know whether a slow moving disease is actually being slowed without something to compare it to. Participants usually keep taking their existing symptom medicines, and many trials offer everyone the real drug afterward, in an extension phase.
See Alzheimer's clinical trials recruiting now
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