发表于 2025年9月22日
If you are like a lot of people, you might be anxious about the risk of getting dementia as you age.
The lifetime risk of developing dementia after age 55 is estimated at 42 percent, according to a 2025 study of over 15,000 participants. The number of Americans developing dementia each year is estimated to increase from 514,000 in 2020 to about 1 million by 2060.
But there have been exciting strides in the diagnosis and treatments for Alzheimer’s, which accounts for 60 to 80 percent of dementia cases, as well as in understanding its biological causes and development. About half of dementia cases may be preventable by addressing known risk factors, according to a 2024 Lancet Commission report.
With these advances, it is important to “press down on the gas pedal and really accelerate this work,” said Ronald Petersen, a professor of neurology and the former director of the Alzheimer’s Disease Research Center at the Mayo Clinic College of Medicine and Science.
“I think we’re at the threshold of making a significant impact on the quality of life — the health span, not just the lifespan,” he said.
Here are some of the exciting advances in dementia research in 2025.
**1. An Alzheimer’s blood test**
In May, the Food and Drug Administration approved the first blood test to detect signals of amyloid beta plaques and tau tangles — the biological hallmarks of Alzheimer’s disease — with over 90 percent accuracy.
“I think this blood biomarker is going to really revolutionize how we diagnose, who can get diagnosed and who’s doing the diagnosis,” said Kristine Yaffe, a professor and the vice chair of the department of psychiatry at the University of California at San Francisco.
For about a decade, clinicians could measure amyloid beta with PET neuroimaging or indications of plaque formation with a lumbar puncture that collects cerebrospinal fluid. But “PET scans are expensive, and lumbar punctures are invasive,” Petersen said. The new blood test can be administered by a primary care provider and represents what some are calling the “democratizing of Alzheimer’s disease diagnostic tests,” he said.
Experts expect that the blood test will make Alzheimer’s diagnostics more accessible, affordable and available in areas where it would otherwise be difficult to receive a clinical diagnosis because of a lack of medical specialists or equipment.
Around the same time as the blood test approval, the Alzheimer’s Association produced the first diagnostic clinical practice guideline using robust scientific literature assessments and incorporating blood-based biomarker tests, said Heather Snyder, the senior vice president of medical and scientific relations at the association.
The blood test measures two key biomarkers of Alzheimer’s disease. One is amyloid beta, a protein that can misfold and create sticky plaques in the brain. The other is p-tau217, an abnormally modified version of tau protein that can lead to the formation of disruptive tangles.
Many biomarkers have been studied, but “p-tau217 seems to be the most informative with regard to the likelihood of the person having underlying Alzheimer’s disease biology,” Petersen said.
Research shows that the p-tau217 biomarker can serve as an warning sign for Alzheimer’s years in advance.
Earlier detection means more opportunity for earlier treatment and intervention, whether with medications or lifestyle changes.
While the buildup of amyloid beta plaques and tau tangles is a hallmark of Alzheimer’s, a positive test does not mean the person necessarily has or will develop Alzheimer’s. (Research has found that more than 20 percent of cognitively unimpaired adults over 65 are amyloid positive.)
Improvements in diagnostics, including the blood test, can also help accelerate research into treatments.
Clinical trials targeting specific biological processes can more precisely enroll patients who have those biological biomarkers, Petersen said.
In the future, just as we get routine tests for cholesterol, we could get a blood test covering different biomarkers to create our unique profile for dementia, which could then be tailored for treatment, he said.
**2. Lifestyle interventions can lead to better cognition**
In July, the largest lifestyle intervention clinical trial in the United States found that simultaneously targeting multiple areas — nutrition, exercise, cognitive training, health monitoring — improved cognitive measures of participants who were at risk of dementia. Participants in the more structured group improved more than those who were self-guided.
The trial, known as U.S. POINTER, was “a big moment” and “culminates decades of research that really informed the intervention,” including a previous lifestyle intervention trial conducted in Finland, said Snyder, one of the POINTER study’s authors.
What’s important is that “there are ways you can reduce your risk factors for having Alzheimer’s disease and other dementias” and “actually can improve your cognitive aging profile,” said Yaffe, who ran a smaller trial on personalized risk reduction in 2024.
For example, a study published in August suggested that people who have a higher genetic risk of developing Alzheimer’s because they carry the APOE4 gene benefit the most from adhering to a Mediterranean diet.
The POINTER trial is expected to yield more insights soon.
About half of the participants volunteered to get neuroimaging, and data on how these lifestyle changes affect the brain are set to be released later this year, Snyder said.
**3. Increasing focus on inflammation**
While amyloid beta continues to be a target of dementia research, scientists are increasingly investigating the role played by inflammation in increasing dementia risk.
“Alzheimer’s is a complex disease, and it’s likely not going to be a single approach,” Snyder said.
Indeed, a study published in July found that people with the APOE4 gene share many changes to their immune system, which may account for their susceptibility to not only Alzheimer’s but also other neurodegenerative diseases.
Inflammation and immune dysfunction cuts across many different neurodegenerative disorders, including dementia and Parkinson’s.
“I think a big push now is on immunomodulation for Alzheimer’s and other degenerative diseases,” said Yaffe, speaking about ways of modifying immune system activity.
**4. Vaccines may reduce dementia risk**
One way we could modify immune system activity linked to reduced dementia risk? Vaccines.
Recently, several large-scale studies compared the outcomes of people who received vaccines to those who did not.
Together, they provide robust evidence that vaccines could fight dementia risk.
In April, one study published in Nature tracked more than 280,000 adults in Wales and found that the shingles vaccine cut the risk of developing dementia by 20 percent over a seven-year period. In June, another study tracking more than 430,000 adults found that vaccines against shingles as well as respiratory syncytial virus (RSV) were associated with reduced dementia risk.
There are two broad biological hypotheses for why vaccines are linked to reduced dementia risk. First, vaccines could reduce the risk of infections, which have been linked to increased dementia risk. Second, the vaccine itself may activate the immune system in a beneficial way.
These two mechanisms are not mutually exclusive and may both play a role, researchers said.
**5. A newly discovered link to lithium**
In August, a study published in Nature reported that the metal lithium may play a protective role in Alzheimer’s.
“The idea that lithium is neuroprotective has been around for a while,” said Yaffe, who was not involved in the study.
In a healthy brain, lithium helps to maintain the proper functioning of neurons. Lithium carbonate is also used to treat bipolar disorder.
The study, which was conducted in mice, found that amyloid beta plaques trapped lithium, rendering it less effective. And low lithium produced an inflammatory environment in the brain and was marked by accelerated accumulation of amyloid beta plaques and tau tangles.
Researchers reported that small amounts of lithium orotate could reverse the disease and restore brain function, which points to an exciting potential therapy to test in humans.
“I think the scientific rationale is compelling and interesting, but we need to really evaluate it in the clinical trial to see if it might be therapeutically useful,” Petersen said.
If you are like a lot of people, you might be anxious about the risk of getting dementia as you age.
如果你和很多人一样,随着年龄增长,你可能会为自己患上痴呆(亦称失智症)的风险而感到焦虑。
The lifetime risk of developing dementia after age 55 is estimated at 42 percent, according to a 2025 study of over 15,000 participants. The number of Americans developing dementia each year is estimated to increase from 514,000 in 2020 to about 1 million by 2060.
根据一项在2025年发表、纳入逾15,000名参与者的研究,55岁之后一生中患上痴呆(dementia)的风险估计为42%。预计美国每年新增痴呆患者的人数将从2020年的514,000人增加到2060年的约1,000,000人。
But there have been exciting strides in the diagnosis and treatments for Alzheimer’s, which accounts for 60 to 80 percent of dementia cases, as well as in understanding its biological causes and development. About half of dementia cases may be preventable by addressing known risk factors, according to a 2024 Lancet Commission report.
但在阿尔茨海默病(占全部痴呆病例的60%至80%)的诊断与治疗方面,以及对其生物学致病原因和发展过程的认识上,已经取得了令人振奋的进展。根据2024年《柳叶刀》委员会(Lancet Commission)的报告,通过应对已知危险因素,大约一半的痴呆病例可能可以被预防。
With these advances, it is important to “press down on the gas pedal and really accelerate this work,” said Ronald Petersen, a professor of neurology and the former director of the Alzheimer’s Disease Research Center at the Mayo Clinic College of Medicine and Science.
梅奥诊所医学院与科学学院神经病学教授、阿尔茨海默病研究中心前主任Ronald Petersen表示:“借助这些进展,我们必须‘把油门踩下去’,真正加速这项工作。”
“I think we’re at the threshold of making a significant impact on the quality of life — the health span, not just the lifespan,” he said.
他说:“我认为我们正处在能对生活质量——也就是健康寿命,而不只是总寿命——产生重大影响的门槛上。”
Here are some of the exciting advances in dementia research in 2025.
以下是2025年痴呆研究的一些令人振奋的进展。
**1. An Alzheimer’s blood test**
1. 阿尔茨海默病血液检测
In May, the Food and Drug Administration approved the first blood test to detect signals of amyloid beta plaques and tau tangles — the biological hallmarks of Alzheimer’s disease — with over 90 percent accuracy.
5月,美国食品药品监督管理局(FDA)批准了首个可检测淀粉样β蛋白斑块和Tau蛋白缠结信号的血液检测——这两者是阿尔茨海默病的生物学标志;该检测的准确率超过90%。
“I think this blood biomarker is going to really revolutionize how we diagnose, who can get diagnosed and who’s doing the diagnosis,” said Kristine Yaffe, a professor and the vice chair of the department of psychiatry at the University of California at San Francisco.
“我认为,这项血液生物标志物(blood biomarker)将真正颠覆我们的诊断方式、谁能够被诊断,以及由谁来进行诊断。”加州大学旧金山分校(University of California at San Francisco)精神病学系教授兼副主任Kristine Yaffe说。
For about a decade, clinicians could measure amyloid beta with PET neuroimaging or indications of plaque formation with a lumbar puncture that collects cerebrospinal fluid. But “PET scans are expensive, and lumbar punctures are invasive,” Petersen said. The new blood test can be administered by a primary care provider and represents what some are calling the “democratizing of Alzheimer’s disease diagnostic tests,” he said.
在过去大约十年里,临床医生可以用PET神经影像测量淀粉样β,或通过腰椎穿刺(采集脑脊液)来判断是否存在斑块形成的迹象。但“PET扫描很昂贵,而腰椎穿刺具有侵入性,”彼得森说。他表示,新的血液检测可以由初级保健医生来实施,有人称之为“阿尔茨海默病诊断检测的民主化”。
Experts expect that the blood test will make Alzheimer’s diagnostics more accessible, affordable and available in areas where it would otherwise be difficult to receive a clinical diagnosis because of a lack of medical specialists or equipment.
专家预计,这种血液检测将使阿尔茨海默病的诊断更易获得、成本更可承受,并能在那些因缺乏医学专科人才或设备而难以获得临床诊断的地区更广泛地开展。
Around the same time as the blood test approval, the Alzheimer’s Association produced the first diagnostic clinical practice guideline using robust scientific literature assessments and incorporating blood-based biomarker tests, said Heather Snyder, the senior vice president of medical and scientific relations at the association.
该协会医疗与科学关系高级副总裁Heather Snyder表示,在血液检测获批的差不多同时期,阿尔茨海默病协会发布了首个诊断用的临床实践指南,该指南基于对科学文献的严谨评估,并将血液生物标志物检测纳入其中。
The blood test measures two key biomarkers of Alzheimer’s disease. One is amyloid beta, a protein that can misfold and create sticky plaques in the brain. The other is p-tau217, an abnormally modified version of tau protein that can lead to the formation of disruptive tangles.
该血液检测衡量阿尔茨海默病的两个关键生物标志物。其一是淀粉样β(amyloid beta),这是一种可能发生错误折叠并在大脑中形成黏性斑块的蛋白质。其二是p-tau217,即tau蛋白的一种异常修饰版本,可能导致形成具有破坏性的缠结(即神经原纤维缠结)。
Many biomarkers have been studied, but “p-tau217 seems to be the most informative with regard to the likelihood of the person having underlying Alzheimer’s disease biology,” Petersen said.
已经有许多生物标志物被研究过,但“就判断一个人是否存在阿尔茨海默病的潜在生物学机制而言,p-tau217 似乎信息量最大,”彼得森说。
Research shows that the p-tau217 biomarker can serve as an warning sign for Alzheimer’s years in advance.
研究显示,p‑tau217 这种生物标志物可以在阿尔茨海默病发病前的数年就作为预警信号。
Earlier detection means more opportunity for earlier treatment and intervention, whether with medications or lifestyle changes.
越早发现,就意味着越有机会尽早进行治疗和干预,无论是通过药物,还是通过调整生活方式。
While the buildup of amyloid beta plaques and tau tangles is a hallmark of Alzheimer’s, a positive test does not mean the person necessarily has or will develop Alzheimer’s. (Research has found that more than 20 percent of cognitively unimpaired adults over 65 are amyloid positive.)
尽管β-淀粉样蛋白斑块和tau缠结的堆积是阿尔茨海默病的标志,但检测呈阳性并不意味着这个人已经患有或一定会发展为阿尔茨海默病。(研究发现,65岁以上且认知功能未受损的成年人中,超过20%为“淀粉样蛋白阳性”。)
Improvements in diagnostics, including the blood test, can also help accelerate research into treatments.
包括血液检测在内的诊断改进,也能加速治疗方面的研究。
Clinical trials targeting specific biological processes can more precisely enroll patients who have those biological biomarkers, Petersen said.
彼得森表示,针对特定生物学过程的临床试验,可以更精准地招募到体内具有这些生物标志物的患者。
In the future, just as we get routine tests for cholesterol, we could get a blood test covering different biomarkers to create our unique profile for dementia, which could then be tailored for treatment, he said.
他说,未来,就像我们现在常规做胆固醇检测一样,我们也可能通过一项覆盖多种生物标志物的血液检测,为痴呆建立个人化的独特“生物学画像”,并据此量身定制治疗方案。
**2. Lifestyle interventions can lead to better cognition**
2. 生活方式干预可以带来更好的认知能力
In July, the largest lifestyle intervention clinical trial in the United States found that simultaneously targeting multiple areas — nutrition, exercise, cognitive training, health monitoring — improved cognitive measures of participants who were at risk of dementia. Participants in the more structured group improved more than those who were self-guided.
7月,美国规模最大的生活方式干预临床试验发现,同时从多个方面入手——营养、运动、认知训练、健康监测——能改善有痴呆风险参与者的认知指标(如记忆与思维能力)。接受更为结构化干预的一组比自我指导的一组改善更明显。
The trial, known as U.S. POINTER, was “a big moment” and “culminates decades of research that really informed the intervention,” including a previous lifestyle intervention trial conducted in Finland, said Snyder, one of the POINTER study’s authors.
POINTER 研究的作者之一 Snyder 表示,这项名为 U.S. POINTER 的试验是“一个重要时刻”,也是“汇聚并完善了数十年来为这种干预提供依据的研究成果”的结晶,其中包括此前在芬兰开展的一项生活方式干预试验。
What’s important is that “there are ways you can reduce your risk factors for having Alzheimer’s disease and other dementias” and “actually can improve your cognitive aging profile,” said Yaffe, who ran a smaller trial on personalized risk reduction in 2024.
Yaffe(她在2024年开展了一项关于个体化风险降低的小型试验)表示,关键在于,“确实有办法降低你患阿尔茨海默病(Alzheimer’s disease)及其他各类痴呆的风险因素”,而且“实际上可以改善你的认知老化状况(即随着年龄增长的认知功能表现)”。
For example, a study published in August suggested that people who have a higher genetic risk of developing Alzheimer’s because they carry the APOE4 gene benefit the most from adhering to a Mediterranean diet.
例如,8月发表的一项研究表明,因携带 APOE4 基因而在遗传上患阿尔茨海默病风险更高的人,从坚持地中海饮食(Mediterranean diet)中获益最大。
The POINTER trial is expected to yield more insights soon.
预计POINTER试验很快会带来更多新的见解。
About half of the participants volunteered to get neuroimaging, and data on how these lifestyle changes affect the brain are set to be released later this year, Snyder said.
Snyder表示,大约一半的参与者自愿接受神经影像学检查(如MRI等),而关于这些生活方式改变如何影响大脑的数据预计将在今年晚些时候发布。
**3. Increasing focus on inflammation**
3. 更加关注炎症
While amyloid beta continues to be a target of dementia research, scientists are increasingly investigating the role played by inflammation in increasing dementia risk.
尽管β-淀粉样蛋白(amyloid beta)仍是痴呆研究的主要靶点,科学家正日益探究炎症在增加痴呆风险中的作用。
“Alzheimer’s is a complex disease, and it’s likely not going to be a single approach,” Snyder said.
“阿尔茨海默病是一种复杂的疾病,很可能不能用单一途径来应对,”Snyder(斯奈德)说。
Indeed, a study published in July found that people with the APOE4 gene share many changes to their immune system, which may account for their susceptibility to not only Alzheimer’s but also other neurodegenerative diseases.
确实,有一项发表于7月的研究发现,携带APOE4基因的人在免疫系统上存在许多共同的变化,这可能解释了他们不仅更易患阿尔茨海默病(Alzheimer’s),也更易罹患其他神经退行性疾病的原因。
Inflammation and immune dysfunction cuts across many different neurodegenerative disorders, including dementia and Parkinson’s.
炎症与免疫功能失调贯穿于多种神经退行性疾病之中,包括痴呆和帕金森病。
“I think a big push now is on immunomodulation for Alzheimer’s and other degenerative diseases,” said Yaffe, speaking about ways of modifying immune system activity.
“我认为,现在的一个重要方向是针对阿尔茨海默病以及其他退行性疾病开展免疫调节,”Yaffe 说,她指的是通过调整免疫系统活性来进行干预的方式。
**4. Vaccines may reduce dementia risk**
4. 疫苗或能降低痴呆风险
One way we could modify immune system activity linked to reduced dementia risk? Vaccines.
我们可以通过什么方式来调节与降低痴呆风险相关的免疫系统活动?——接种疫苗。
Recently, several large-scale studies compared the outcomes of people who received vaccines to those who did not.
近期,数项大规模研究对比了接种疫苗人群与未接种人群的健康结局。
Together, they provide robust evidence that vaccines could fight dementia risk.
综合而言,它们共同提供了有力的证据,表明疫苗可能有助于降低痴呆的风险。
In April, one study published in Nature tracked more than 280,000 adults in Wales and found that the shingles vaccine cut the risk of developing dementia by 20 percent over a seven-year period. In June, another study tracking more than 430,000 adults found that vaccines against shingles as well as respiratory syncytial virus (RSV) were associated with reduced dementia risk.
4月,一项发表在《Nature(自然)》上的研究追踪了威尔士逾28万名成年人,发现接种带状疱疹疫苗在7年内可将患痴呆的风险降低20%。6月,另一项追踪逾43万名成年人的研究发现,针对带状疱疹以及呼吸道合胞病毒(RSV)的疫苗与较低的痴呆风险相关。
There are two broad biological hypotheses for why vaccines are linked to reduced dementia risk. First, vaccines could reduce the risk of infections, which have been linked to increased dementia risk. Second, the vaccine itself may activate the immune system in a beneficial way.
关于疫苗为何与降低痴呆(即失智症)风险相关,主要有两种生物学假说。其一,疫苗可以降低感染风险,而感染与痴呆风险升高有关。其二,疫苗本身可能以一种有益的方式激活免疫系统。
These two mechanisms are not mutually exclusive and may both play a role, researchers said.
研究人员表示,这两种机制并不相互排斥,二者可能都会发挥作用。
**5. A newly discovered link to lithium**
5. 新发现:与锂的关联
In August, a study published in Nature reported that the metal lithium may play a protective role in Alzheimer’s.
8月,《Nature》(《自然》)发表的一项研究报告称,金属锂可能在阿尔茨海默病中发挥保护作用。
“The idea that lithium is neuroprotective has been around for a while,” said Yaffe, who was not involved in the study.
“锂具有神经保护作用这一观点已经存在一段时间了,”未参与该研究的Yaffe说。
In a healthy brain, lithium helps to maintain the proper functioning of neurons. Lithium carbonate is also used to treat bipolar disorder.
在健康的大脑中,锂有助于维持神经元的正常功能。碳酸锂也用于治疗双相情感障碍(bipolar disorder)。
The study, which was conducted in mice, found that amyloid beta plaques trapped lithium, rendering it less effective. And low lithium produced an inflammatory environment in the brain and was marked by accelerated accumulation of amyloid beta plaques and tau tangles.
该研究在小鼠中进行,发现淀粉样β(amyloid beta)斑块会“捕获”锂,从而削弱其作用。而且,当体内锂水平较低时,会在大脑中形成一种炎性环境,并伴随淀粉样β斑块和tau缠结(tau tangles)的加速堆积。
Researchers reported that small amounts of lithium orotate could reverse the disease and restore brain function, which points to an exciting potential therapy to test in humans.
研究人员报告,少量乳清酸锂(lithium orotate,乳清酸为乳清酸/乳清嘧啶酸)可逆转该疾病并恢复脑功能,这指向了一种令人振奋、值得在人类中开展试验的潜在疗法。
“I think the scientific rationale is compelling and interesting, but we need to really evaluate it in the clinical trial to see if it might be therapeutically useful,” Petersen said.
“我认为其科学依据令人信服且颇为有趣,但我们需要在临床试验中进行真正的评估,看看它是否具有治疗上的价值。”彼得森说。