Every day it seems scientists are making breakthroughs in Alzheimer\u2019s disease.<\/p>\n
New treatments that actually slow the disease\u2019s progression \u2014 lecanemab and donanemab \u2014 have finally appeared on pharmacy shelves<\/a> in the past few years, delivering real-world results for patients and their families. New blood tests promise<\/a> to identify at-risk patients earlier in their lives, giving them the chance to make lifestyle changes and potentially start treatment to stave off symptoms.<\/p>\n The media and wellness influencers are always reporting<\/a> on new diets, workouts, or hobbies that can combat dementia. Just last month, there was even a report out of China<\/a> about an experimental brain surgery that allegedly reverses the symptoms of Alzheimer\u2019s disease \u2014 the Holy Grail that researchers have been pursuing for generations.<\/p>\n But hype has outpaced the science of treating Alzheimer\u2019s disease before. Promising treatments have gotten a lot of attention before only to fizzle out<\/a> a short time later. Less than a decade ago, many scientists were wondering<\/a> whether we had the theory of Alzheimer\u2019s disease completely wrong.<\/p>\n For those of us who don\u2019t work in the field, that confusing history can make it hard to make sense of these recent developments. It sounds like we are entering a new age for Alzheimer\u2019s prevention and treatment \u2014 but are we actually? And, if we are, how can people benefit from it?<\/p>\n I called a couple of leading experts to find out.<\/p>\n Here\u2019s the good news: They say scientists are genuinely shifting the paradigm for treating, detecting, and ultimately preventing Alzheimer\u2019s disease. The two drugs on the market can actually slow down cognitive decline for many patients, something that had been out of reach for decades. And more treatments are coming.<\/p>\n \u201cDiagnosis and treatment of Alzheimer\u2019s has changed in a way that is revolutionary compared to, say, four or five years ago,\u201d said Dr. Jason Karlawish, co-director of the Penn Memory Center.<\/p>\n At the clinic where he sees patients, \u201cpeople are feeling a sense of hope and promise,\u201d he said.<\/p>\n For a long time, the science on Alzheimer\u2019s disease felt stuck. Now it\u2019s moving. There\u2019s only one thing that could stop it, according to experts: the Trump administration\u2019s anti-science agenda.<\/p>\n Scientists are getting closer to game-changing Alzheimer\u2019s treatments<\/p>\n In 2023, the approval of two drugs transformed the landscape of Alzheimer\u2019s care: lecanemab<\/a> (sold as Leqembi) and donanemab<\/a> (sold as Kisunla), two IV treatments that target amyloid plaque in the brain of a person with Alzheimer\u2019s. Before these two drugs \u2014 and the approval of aducanemab<\/a>, a similar but less effective and riskier treatment \u2014 it had been decades since the last new Alzheimer\u2019s treatment had come onto the market.<\/p>\n They are not perfect treatments. They are effective only for people with mild cognitive impairment, not more advanced stages of the disease. They can only slow the progression of Alzheimer\u2019s for those people, not stop or reverse it. And they do come with the risk of serious side effects, particularly brain bleeds.<\/p>\n \u201cThe good news is, we have these two drugs that can help people,\u201d said Tara Spires-Jones, professor of neurodegeneration at the University of Edinburgh and author of the forthcoming book, Fighting for our Minds: The Neuroscience of Defeating Dementia<\/a>. \u201cThe bad news is, you don\u2019t get any better. You\u2019re still getting worse \u2014 you just get worse more slowly.\u201d<\/p>\n These drugs are a start, not the endpoint. Researchers are already working on the next generation of treatments. The drug pipeline is becoming more robust because scientists are finally coalescing around a theory of the disease that\u2019s more complex \u2014 and, crucially, opens more potential targets for new drugs.<\/p>\n For a long time, Alzheimer\u2019s research was dominated by the amyloid hypothesis<\/a>. The theory posited that the buildup of plaque made from amyloid proteins was responsible for disrupting brain signals and creating the telltale loss of memory and identity associated with Alzheimer\u2019s. Scientists are still confident that amyloid plays a role in Alzheimer\u2019s \u2014 and the success of these amyloid-targeting drugs supports that interpretation. But there is also a stronger consensus that other mechanisms must be at work. Some people who have evidence of amyloid plaque building up in their brain nonetheless never develop Alzheimer\u2019s disease.<\/p>\n Another type of protein called tau seems to be associated with the disease. Scientists also increasingly believe that inflammation may play a role. Part of the breakthrough of the past few years is that scientists are no longer arguing about whether they even understand this disease at all. Instead, the mission is to pursue different drug targets and increase the chances of delivering new treatments.<\/p>\n \u201cI don\u2019t think people in the field are fighting over, \u2018Your mechanism is wrong and mine is right,\u2019\u201d Karlawish said. \u201cI think there\u2019s a kind of general democratization. There are multiple promising mechanisms.\u201d<\/p>\n New tau-targeting treatments are moving through clinical trials. Biogen has a drug called diranersen<\/a> that aims to stop the production of the tau proteins moving through clinical trials. Preliminary results showed<\/a> that the drug did appear to reduce tau and improve cognitive symptoms \u2014 although, curiously, the most effective response was at the lowest dose. Further research is needed before the drug could receive FDA approval. Another tau-targeting drug from Eisai has also entered clinical trials<\/a> and is in the earlier safety-check phases. And new amyloid-targeting treatments<\/a> aim to better penetrate the brain-blood barrier and deliver more effective relief for patients.<\/p>\n In the short term, scientists hope these drugs can slow or even stop cognitive decline better than the currently approved medications. In the longer term, these new approaches \u2014 and potentially a combination of different drugs with different targets \u2014 could eventually allow scientists to reverse Alzheimer\u2019s. (As for that experimental surgery in China, as Nature reported<\/a>, scientists say its results will need to be replicated in other clinical trials before we\u2019re confident that it really works.)<\/p>\n \u201cThe brain is amazing. You can make new synapses,\u201d Spires-Jones said. \u201cIf we could stop the insult, it\u2019s theoretically possible in the future that we could have treatments that not only slow the progression but actually let you get better. But I think we\u2019re pretty far from those. What I think is much closer is really, really meaningful treatments that will slow or even stop disease progression. We\u2019re probably going to see something coming out in the next couple of years.\u201d<\/p>\n How patients can get the most out of these new treatments<\/p>\n But even a \u201ccure\u201d in the long term will be conditional. Because Alzheimer\u2019s eventually causes the brain to die (thus its 100 percent fatality rate), there may still be a point of no return once the disease is too entrenched. \u201cA cure for people in the late stages is practically impossible because too much of the brain has died,\u201d Spires-Jones said.<\/p>\n And that reality makes early detection all the more important. That\u2019s the way patients can get the most out of the current medications and their eventual successors.<\/p>\n It used to be that doctors couldn\u2019t confirm whether somebody had Alzheimer\u2019s disease until the person died and they could perform an autopsy. But the new treatments can give people more time with their loved ones before the disease\u2019s worst symptoms kick in.<\/p>\n That means waiting is not an option. Patients are demanding better methods of detection.<\/p>\n \u201cTreatment attracts patients, for good reason, and treatment demands diagnosis,\u201d Karlawish said. \u201cTreatment really does drive the business model for a disease.\u201d<\/p>\n So, scientists are designing<\/a> new blood tests that can detect the presence of tau proteins<\/a> and predict the later onset of Alzheimer\u2019s disease<\/a> with impressive accuracy. And they are learning more about pivotal periods in a person\u2019s life where their risk of Alzheimer\u2019s might start to grow \u2014 and when interventions might therefore be more effective. New research has suggested<\/a> that menopause may be an accelerant for Alzheimer\u2019s progression, and therefore may represent an important point in someone\u2019s life.<\/p>\n These developments are shaping what the near-term future of Alzheimer\u2019s care will look like. As a person ages, they will be able to take one of these blood tests to see if there are signals they are at a higher risk of the disease. If they are, they will have a growing number of medications that they could take to delay or potentially prevent dementia from setting in. For a woman at risk, for example, hormone replacement therapy has been associated<\/a> with a reduced risk of dementia. Clinical trials are also underway to test whether existing drugs like donanemab<\/a> and lecanemab<\/a> can delay the onset of symptoms for somebody who is at higher risk but has not yet started to experience cognitive decline.<\/p>\n \u201cWe couldn\u2019t get the right people at the right time early on \u2014 and now we can,\u201d Spires-Jones said. \u201cThat\u2019s a problem that\u2019s almost solved now.\u201d<\/p>\n Prevention may also be where GLP-1 drugs ultimately prove most useful. As scientists come to better understand the intimate relationship between vascular health and brain health, there is growing reason to think these medicines could help reduce dementia risk decades before symptoms appear.<\/p>\n That would make GLP-1s a complement to drugs such as lecanemab and donanemab, rather than a competitor. Those treatments are designed for people who already have early-stage Alzheimer\u2019s. GLP-1s, by contrast, have so far shown little ability to slow the disease once cognitive decline has begun. In a disappointing clinical trial<\/a> involving people with mild cognitive impairment or early Alzheimer\u2019s, researchers found that the drugs had a negligible effect on the progression of the disease.<\/p>\n But that result doesn\u2019t mean there isn\u2019t a role for Ozempic and the next generation of GLP-1 drugs in the fight against Alzheimer\u2019s.<\/p>\n Scientists increasingly believe that chronic inflammation, obesity, and poor vascular health can all accelerate cognitive aging. GLP-1 drugs reduce inflammation<\/a>, while their effects on weight and metabolic health can substantially lower cardiovascular risk<\/a>. If US obesity rates continue to fall<\/a> as these medicines become more widely used, their most consequential effect on Alzheimer\u2019s may therefore be indirect: improving the health of millions of people long before the disease takes hold.<\/p>\n \u201cI think where we\u2019re going in the future is those semaglutide-type drugs will probably be very good for prevention,\u201d Spires-Jones said. \u201cIf we can keep people\u2019s obesity in check, that will probably more likely be a preventative treatment. That trial pretty conclusively told us that once you have symptoms, at least, that drug is not going to help.\u201d<\/p>\n This summer, the Alzheimer\u2019s Association announced<\/a> a $100 million research project to examine whether lifestyle changes plus a GLP-1 medication could reduce the risk of dementia in at-risk older adults.<\/p>\n If you\u2019re worried about your own cognitive health or that of a loved one, you have options, and those options are only going to grow. Talk to your doctor. There are FDA-approved blood tests<\/a> you can already take. Ask about lecanemab and donanemab. You may also be a good candidate to help scientists in the most active areas of development. Researchers need people to participate in their clinical trials. The Alzheimer\u2019s Association<\/a> and the federal government<\/a> have online tools to help people find clinical trials that you or someone you love could be a candidate for.<\/p>\n Science funding cuts could slow down this progress<\/p>\n All the optimism about the future of Alzheimer\u2019s treatment is based on research and clinical trials. When I asked Karlawish and Spires-Jones about where the story goes from here, they shared one concern: that science becomes so politicized that it would be difficult to get grant funding for research projects that could lead to additional breakthroughs.<\/p>\n \u201cIn some sense, the biggest threat is outside the science,\u201d Karlawish said. \u201cThere\u2019s deep concern that this politicization of the grant process will essentially wreck American science. We can\u2019t sustain that kind of environment and still demand the results that we\u2019ve come to expect.\u201d<\/p>\n President Donald Trump and US Health Secretary Robert F. Kennedy Jr. like to present their crusade to reform American science as being targeted at frivolous DEI projects. But there are already examples of serious dementia studies being affected: Last month, the Trump administration canceled<\/a> $15 million in grants for studies to evaluate how discrimination affects long-term brain health.<\/p>\n This is another place where we have more agency to impact what happens next: the ballot box. Use your individual political power to support lawmakers who defend the scientists and researchers doing critical work.<\/p>\n \u201cYou can vote for people who will fund and support science as an endeavor,\u201d Spires-Jones said. \u201cAdvances in science don\u2019t happen on their own. We need all of society to get involved.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"Every day it seems scientists are making breakthroughs in Alzheimer\u2019s disease. 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