The Disease That Starts Before You Notice
Alzheimer's Awareness Month
Alzheimer's doesn't begin when symptoms appear. The biological damage starts years, sometimes decades, earlier — and the disease is no longer as invisible as it once was.
June is Alzheimer's & Brain Awareness Month, and the conversation about the disease tends to undermine it. People talk about memory loss, about forgetting names and faces, about the worst of it. They skip over everything that comes before. That's the more important part.
Alzheimer's is a disease affecting over 55 million people worldwide. The biological damage starts years, sometimes decades, before symptoms appear. Two proteins are responsible for most of it: and .
Amyloid-beta is a produced naturally during normal neuronal activity. In a healthy brain, it gets cleared. In Alzheimer's, it doesn't. The peptide misfolds, clumps together, and forms between neurons. Tau is a separate protein that normally stabilizes , the structural tracks neurons use to transport nutrients. In Alzheimer's, tau becomes , detaches from those tracks, and aggregates into inside the cell. Together, these plaques and tangles drive , , and cell death.
For most of modern medicine, you couldn't confirm this pathology in a living person. Diagnosis relied on clinical symptoms, cognitive tests, and inference. changed that, letting clinicians track and tau accumulation in living patients. Blood tests introduced in 2024 go further: they match PET results more than 90% of the time, and at a fraction of the cost and accessibility barrier. That matters because the treatments currently available only work in the early stages.
In 2023, the FDA granted full approval to , a that targets and clears amyloid from the brain. followed in July 2024, with a monthly infusion schedule and the possibility of stopping treatment once scans confirm the brain is amyloid-free. These are the first therapies that address the underlying disease biology rather than the symptoms. They aren't cures. They slow progression. But for a disease that had no disease-modifying treatment for over a century, that's not nothing.
Both treatments are limited to early-stage patients, which is exactly why the diagnostic advances matter. They're most effective during or early dementia, and they're unlikely to reverse extensive neuronal damage in later stages. You can't benefit from a treatment window you never knew you were in.
There's also growing attention toward tau-targeting therapies. Anti-amyloid approaches proved the concept that clearing pathological proteins can slow decline, but the tau pipeline struggled through late 2025. Posdinemab was discontinued after its Phase 2 trial showed no cognitive benefit. Etalanetug showed promising reductions in tau levels in the blood in a small early study, but larger trials are still ongoing. The field is still working out whether clearing tau translates to clinical improvement the way amyloid clearance has.
Something I keep coming back to: this disease, which most people associate with the later years of life, is actually a slow accumulation problem that begins in midlife or earlier. The 2024 Lancet Commission identified 14 modifiable risk factors that, if addressed, could reduce dementia cases by 45%. Hearing loss, social isolation, high LDL cholesterol, and physical inactivity. Things that seem disconnected from brain disease, but aren't.
The biology is getting clearer. The diagnostics are getting cheaper. The treatments are imperfect but real. Five years of progress have moved faster than the several decades before them, and the disease is no longer as invisible as it once was.