Alzheimer’s Disease Treatment: A Turning Point, But Not the Finish Line

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Alzheimer’s disease treatment has entered a new era. For the first time, therapies that target the biology of the disease are changing what researchers, clinicians, patients, and families can expect from treatment.

In a new Open Access review published in the Journal of Neurochemistry, Sir John Hardy explores why the approval of the anti-amyloid antibodies lecanemab and donanemab marks an important turning point, and why the field still faces major challenges before Alzheimer’s disease can be safely and more effectively treated. The review, Alzheimer’s Disease: Treatment Challenges for the Future, discusses what these therapies mean for disease biology, diagnosis, safety, and the future direction of Alzheimer’s research.

Why Anti-Amyloid Antibodies Matter in Alzheimer’s Disease

Alzheimer’s disease is strongly linked to the build-up of amyloid plaques and tau tangles in the brain. These changes are widely recognised as key features of the disease and are central to how researchers understand Alzheimer’s progression.

For decades, scientists debated whether amyloid was truly a main driver of Alzheimer’s disease or only one part of a much larger process. The arrival of anti-amyloid antibodies has changed that discussion.

Lecanemab and donanemab are designed to remove amyloid from the brain. The FDA converted lecanemab to traditional approval after confirming clinical benefit, and later approved donanemab for adults with Alzheimer’s disease.

For Hardy, this is important because it gives strong support to the idea that amyloid plays a meaningful role in Alzheimer’s disease. But it also shows that removing amyloid is not enough on its own.

Lecanemab and Donanemab: Progress, Not a Cure

The most important message from the review is clear: current Alzheimer’s treatments can slow disease progression, but they do not stop it.

That difference matters.

Slowing decline may give patients and families more time. It may also help people stay independent for longer. But because the disease continues to progress, researchers now need to understand what is still driving decline after amyloid has been reduced.

Hardy highlights this as one of the biggest questions for the next stage of Alzheimer’s research. If amyloid is being removed, why do symptoms continue to worsen? The answer may involve other processes, including tau pathology, inflammation, changes in blood vessels, or the long-term behaviour of microglia, the immune cells of the brain.

This is why the review is so valuable: it does not simply celebrate a breakthrough. It asks what the breakthrough teaches us, and what remains unsolved.

ARIA and the Safety Challenges of Alzheimer’s Treatment

The review also explains why these new treatments are not simple to deliver.

One major concern is ARIA, or amyloid-related imaging abnormalities. ARIA can involve swelling or bleeding in the brain and is a known risk linked to anti-amyloid antibody treatment. Because of this, patients may need regular MRI monitoring and specialist clinical care. The EMA describes ARIA as a recognised serious side effect of lecanemab and notes that people with two copies of the APOE4 gene have a higher risk.

This creates practical challenges. Treatment may involve genetic testing, brain scans, specialist appointments, and careful monitoring over time. These requirements can be demanding for patients, caregivers, clinicians, and healthcare systems.

Hardy points to several possible ways forward, including safer drug design, better delivery methods, earlier treatment, and the possibility of treatment breaks, sometimes called “drug holidays”, once amyloid has been removed. These ideas could help reduce cost, risk, and burden in the future.

Why Earlier Alzheimer’s Diagnosis Is Essential

Current anti-amyloid therapies are mainly intended for people in the early stages of Alzheimer’s disease. This makes early and accurate diagnosis essential.

Today, diagnosis can involve PET scans or cerebrospinal fluid testing. These tools can be useful, but they may also be expensive, invasive, or difficult to access. Biomarkers are therefore becoming increasingly important in Alzheimer’s research and clinical care.

The National Institute on Aging explains that commonly used Alzheimer’s biomarkers include beta-amyloid, tau, and phospho-tau, which can support diagnosis and help researchers detect disease changes earlier.

Hardy highlights blood-based biomarkers as one of the most promising areas for future progress. If reliable blood tests can help identify Alzheimer’s disease earlier and more widely, they could make treatment more accessible and improve how patients are selected for therapy.

However, the review also stresses an important point: these tools must work across diverse populations. Much of the existing clinical trial and biomarker data comes from limited population groups. Future research needs to make sure diagnosis and treatment are reliable for everyone.

What Comes Next for Alzheimer’s Disease Research?

Hardy’s review makes the future of Alzheimer’s treatment feel both hopeful and realistic.

The field has turned a corner. Researchers now have therapies that can change the biology of Alzheimer’s disease, not only treat symptoms. But the next challenge is to make these therapies safer, easier to deliver, more accessible, and more effective.

The review identifies several priorities for the years ahead:

• improving treatment safety
• reducing the burden of MRI monitoring
• developing better biomarkers for early diagnosis
• understanding why decline continues after amyloid removal
• studying treated patients over the long term
• testing therapies in more diverse populations
• exploring whether treatment breaks may be possible

This is what makes the review important. It explains that the approval of lecanemab and donanemab is not the end of the Alzheimer’s story. It is the beginning of a new chapter.

A New Chapter for Alzheimer’s Disease Treatment

Alzheimer’s disease remains one of the most difficult conditions in neuroscience and medicine. But the approval of anti-amyloid antibodies has changed the field.

These treatments are not perfect. They carry risks, require careful monitoring, and do not stop the disease. Yet they show that targeting the mechanisms of Alzheimer’s disease can make a measurable difference.

For researchers, this opens the door to better therapies. For clinicians, it raises new questions about diagnosis, safety, and patient selection. For patients and families, it offers cautious hope — while reminding us that much more work is still needed.

As Hardy argues in this Journal of Neurochemistry review, Alzheimer’s treatment has reached a turning point. The next goal is to move from slowing disease to safely stopping it.

Read the full Open Access review in the Journal of Neurochemistry.