It’s tempting—perhaps even a little too tempting—to herald the release of a new drug like donanemab as a kind of definitive milestone, a breakthrough (that overused word) in the vast, foggy, and ultimately tragic landscape of Alzheimer’s disease, where hope is more often than not met with a footnote of ‘but.’ And yet, here we are, in the wake of new trial results, poised to do just that—but with one eye still on the fine print. According to the findings published in the Journal of the American Medical Association (JAMA) (i.e., a journal whose title alone conveys that we’re supposed to take this very seriously), donanemab has successfully slowed the rate of cognitive decline in patients with early-stage Alzheimer’s by an almost unbelievable 35%. Think about that for a second: 35%. That’s not just a statistic; that’s the difference between being able to still find your keys on a Tuesday morning versus forgetting where you live by next summer.

But of course, this is the point where we insert the ‘but’. Because as much as we want to hold onto that headline figure, there’s the underlying reality of the drug’s side effects—the kind that remind us that even a breakthrough in medicine isn’t exactly a ‘win’ in the uncomplicated, feel-good sense. For every patient whose memory might slow its inevitable unraveling, there’s the sobering statistic that 24% of participants experienced serious side effects. And by serious, we mean brain swelling and other ominous complications that, for four individuals in the trial, led to death. These numbers hang like an asterisk over the entire celebration, because what is scientific progress if it comes at a steep cost to the very people it’s supposed to help?

The Science Behind the Hope (and Caution)

Now, it’s important to understand what exactly donanemab is doing here. We’re told that it’s an immunotherapy drug, which means it’s essentially turning the body’s immune system into a kind of guided missile aimed at the sticky amyloid plaques in the brain—the very plaques that are widely believed to choke off the brain’s ability to function. If this sounds vaguely miraculous, well, it sort of is—except for the fact that this drug works primarily for those in the early stages of the disease. Once Alzheimer’s has progressed to more moderate or severe stages, it’s like trying to close the barn door after the horse has already bolted, gone to another town, and applied for a job as an accountant.

The TRAILBLAZER-ALZ 2 Phase 3 trial (a title that would not be out of place as a subtitle for the next “Fast and Furious” sequel) involved almost 1,800 participants. These were people whose lives had already started to fray at the edges, cognitively speaking, but for whom this treatment might offer the chance to delay the inevitable. And that’s really the crux of it: delay. We’re not talking about a cure here, but rather a temporary stay of execution, a slowing of the disease’s inexorable march. The irony, of course, is that the very thing we celebrate—the drug’s ability to slow decline—requires a level of vigilance (regular infusions, close monitoring) that itself could be exhausting for patients who already find day-to-day life difficult.

Progress Wrapped in Risk: The Complicated Role of Side Effects

It would be disingenuous to talk about donanemab without addressing the darker side of its success. 24% of trial participants experienced what we might politely call “complications,” though complications feels like an understatement when the side effects include brain swelling—a condition that’s just as unsettling as it sounds. Add to that the fact that four people died during the trial, with their deaths directly tied to the drug’s side effects, and we’re left with a rather unnerving reality. Here we have a drug that can potentially give people back parts of themselves—memories, functions, pieces of identity that Alzheimer’s would otherwise rip away—but at what cost? And who gets to decide what cost is too high?

As Professor John O’Brien put it, these results represent a real “breakthrough” in Alzheimer’s treatment, but he’s quick to temper the celebration with words like “caution” and “monitoring”. In a statement that seems to walk a delicate line between hope and realism, he reminds us that the clinical benefits, while significant, are modest, and that these drugs may not be suitable for most people with Alzheimer’s. “Some caution is needed,” he says, which, when translated from medical-ese, means: don’t expect a miracle. Yes, it’s a step in the right direction, but it’s also just the first step in a marathon.

The Road Ahead: Breakthrough or Just the Beginning?

It’s worth noting that donanemab is not the first of its kind to show promise. Last year, a similar drug—lecanemab—also slowed cognitive decline, though by a slightly lower margin (27% versus 35%). Together, these drugs represent what scientists love to call proof of principle—in other words, they show that it’s possible to target the disease at a molecular level. This is exciting because, for so long, Alzheimer’s has been the disease where treatments were more about managing symptoms than actually modifying the disease itself.

But here’s where we return to the idea of tempered expectations. Donanemab, like its predecessors, doesn’t work for everyone, and even when it does, it’s a slow, incremental benefit. We’re not curing Alzheimer’s; we’re trying to outpace it—however slightly, however temporarily. And for those caught in its early stages, a drug like this might offer just enough time to hold on to what’s slipping away.

And so, while we celebrate the advent of donanemab, we do so knowing full well that scientific breakthroughs—especially in the realm of diseases like Alzheimer’s—are always accompanied by a deep, uncomfortable complexity. Yes, we’ve made progress, but it’s progress with an asterisk, one that reminds us that every step forward is fraught with risk, uncertainty, and—most of all—the hope that the next step will be better.