For most of the 20th century, doctors had little more than compassion to offer patients with Alzheimer’s. But in recent decades, advances in brain imaging and biomarker testing have allowed scientists to track Alzheimer’s pathology as it unfolds — often decades before symptoms appear.
It starts with the slow buildup of beta-amyloid proteins. On their own, these proteins aren’t harmful. But early in the disease process, they begin to clump into toxic plaques in the brain. This sets off a cascade: Tau proteins — which help transport nutrients and signals in brain cells — begin to tangle, disrupting cell function. The brain’s immune system overreacts. Neurons die. And eventually, symptoms emerge — including memory loss, confusion, and changes in behavior or personality.
For years, available treatments only addressed these symptoms. But the approval of anti-amyloid antibodies like Leqembi and Kisunla marked a turning point. These are the first disease-modifying therapies — medications that aim to slow the progression of Alzheimer’s by targeting its underlying biology.
What makes a treatment “disease-modifying”?
In the 1990s and early 2000s, cholinesterase inhibitor drugs like Aricept (donepezil), Exelon (rivastigmine), Razadyne (galantamine), and Namenda (memantine) were approved. These medications help ease cognitive symptoms by boosting brain chemicals involved in learning and memory. For some patients, they offer temporary improvement or stabilization. But over time, the disease continues to progress at the same pace.
That’s where disease-modifying therapies come in. Leqembi and Kisunla target beta-amyloid — one of the earliest drivers of Alzheimer’s. By removing toxic amyloid plaques from the brain, these drugs are designed to interrupt the disease process itself, not just manage the symptoms it causes.
They don’t stop Alzheimer’s, but they do appear to slow it down modestly over an 18-month period. Doctors are hopeful that this slowing effect may grow over time, and ongoing studies are tracking patients to learn more. Because these drugs work best in the early stages of the disease, clinical trials are now testing whether they might also help prevent Alzheimer’s in people with beta-amyloid buildup but no symptoms.
What other treatments are in the pipeline?
Researchers are continuing to develop next-generation anti-amyloid drugs — like remternetug and trontinemab, which are now in late-stage clinical trials. Others are aiming at different targets, like tau tangles or the brain’s immune response, both of which contribute to the spread and severity of Alzheimer’s. These approaches are promising but still several years away.
Interestingly, recent data suggests that galantamine — traditionally seen as a symptom-relieving drug — may also reduce the risk of severe dementia. That’s led some researchers to revisit its potential as a disease-modifying therapy as well.
What this means for patients
While disease-modifying treatments offer new hope, many experts believe that no single drug will be enough to combat such a complex disease. A more likely future: personalized treatment plans that combine therapies targeting the disease process with others that manage symptoms and support quality of life.
Alzheimer’s is no longer untreatable. But progress still depends on early diagnosis, clinical research, and a deeper understanding of how — and when — to intervene.
