Alzheimer's disease is the most common cause of dementia, affecting more than 6 million Americans. Until recently, approved treatments only managed symptoms temporarily. Two new antibody drugs that clear amyloid plaques from the brain—aducanumab and lecanemab—mark the first therapies shown to slow cognitive decline, though the effect is modest and not everyone qualifies.
What's actually going on in research
Trials are testing drugs that target tau tangles, reduce inflammation in the brain, and protect nerve cells from damage. Researchers are also studying combination therapies that address both amyloid and tau, lifestyle interventions that may delay onset, and blood tests that could detect Alzheimer's years before symptoms appear. Some trials focus on people with genetic risk or early biomarker changes.
Anti-tau antibodies
Several antibodies targeting tau protein tangles are in late-stage trials. Since tau damage correlates more closely with cognitive decline than amyloid plaques, these drugs may preserve memory better than current options.
Inflammation control
Drugs that calm overactive immune cells in the brain are showing promise in early trials. Chronic brain inflammation appears to drive neurodegeneration, making it a new therapeutic target.
Blood biomarker tests
Simple blood tests that detect amyloid and tau are becoming accurate enough for clinical use. They could enable earlier diagnosis and help identify who might benefit from treatment before significant damage occurs.
What to know before you search
Eligibility typically depends on cognitive test scores, confirmation of amyloid plaques through PET scan or spinal fluid, genetic status for APOE4, and absence of other dementia causes or significant vascular disease.
What types of trials are currently open
- Anti-amyloid trials — Testing antibodies that remove amyloid plaques from the brain, typically through monthly or biweekly infusions. Participants need regular MRI monitoring for brain swelling or bleeding.
- Anti-tau trials — Testing drugs that target tau tangles or prevent tau from spreading between brain cells. These may work in people with more advanced disease than anti-amyloid drugs.
- Prevention trials — Testing whether treatments can delay or prevent Alzheimer's in people with genetic risk, family history, or early biomarker changes but no symptoms yet.
- Combination trials — Testing multiple drugs together—often an anti-amyloid drug plus an anti-tau drug or anti-inflammatory—to see if targeting several problems at once works better.
- Lifestyle intervention studies — Studies examining whether exercise, diet changes, cognitive training, or managing cardiovascular risk can slow cognitive decline or reduce Alzheimer's risk.
Recently added Alzheimer's Disease trials
Using Light Therapy for Mild Cognitive Impairment
The goal of this clinical trial is to test whether transcranial photobiomodulation (tPBM), a non-invasive brain stimulation technique using near-infrared light, can improve brain blood flow regulation (neurovascular coupling) and cognitive function in people with mild cognitive impairment (MCI). The main questions it aims to answer are: * Does tPBM enhance cognitive function and cerebral hemodynamic responses during memory and finger tapping tasks? * Does tPBM reduce oxidative stress, inflammation, and mitigate brain cell damage? * Is cognitive improvement linked to amyloid status, greater cerebral hemodynamic response, and lower levels of brain inflammation and oxidative stress? Researchers will compare an active tPBM treatment arm to a sham treatment arm to see if tPBM leads to measurable improvements in brain activity and cognitive function compared to no active stimulation. Participants will: * Receive a 20-minute-long active tPBM or sham stimulation session once per day, 6 times per week, for 12 weeks. * Complete questionnaires and an iPad-based cognitive testing protocol. * Complete memory and motor tasks while their brain activity is measured using non-invasive techniques: simultaneous functional near-infrared spectroscopy (fNIRS) and electroencephalography (EEG). Dynamic analysis of the vessels in the eye will also be performed based on eligibility. Transcranial Doppler (TCD) flowmetry is optionally performed. * Provide blood samples to test for biomarkers of inflammation, oxidative stress, and brain cell damage.
Interleukine-2 (IL-2) Plus Semaglutide in Alzheimer's Disease
Alzheimer's disease (AD) is the most common cause of dementia. Despite major research efforts, effective treatments that slow or stop disease progression remain limited. Growing evidence suggests that inflammation in the brain and the body plays a key role in the onset and progression of AD. In particular, immune cells called regulatory T cells (Tregs), which normally help control inflammation, are impaired in AD individuals. This leads to increased activity of harmful immune pathways that worsen brain injury. Interleukin-2 (IL-2) is a drug that can restore the function of Tregs. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as semaglutide, are a class of drugs currently used to treat diabetes and obesity. Beyond their metabolic effects, GLP-1RAs also reduce inflammation, protect brain cells, and improve cellular energy balance. Laboratory studies, including our own, show that combining IL-2 with semaglutide has stronger effects than either drug alone. Together, they enhance Treg function, dampen harmful inflammatory responses, and improve cell survival. These findings support testing IL-2 plus semaglutide as a novel combination therapy for AD. We now propose a clinical trial to evaluate the safety, feasibility, and biological effects of this strategy. The study will enroll 30 individuals with AD, ages 50 to 86, who have a confirmed diagnosis by amyloid PET brain imaging and a Mini-Mental State Exam score between 16 and 26. Participants will be randomly assigned to one of three groups: (1) placebo, (2) low-dose IL-2 alone, or (3) IL-2 combined with semaglutide. Throughout the trial, participants will undergo regular medical exams, blood tests, and safety monitoring. We will measure how the treatment affects Tregs and other immune cells, inflammatory markers in blood and CSF, and established Alzheimer's biomarkers such as amyloid beta, tau, and neurofilament light chain. Cognitive and functional assessments will also be conducted to explore potential benefits on memory and daily living skills. If successful, this study will provide the first evidence that a dual immunotherapeutic strategy can safely modify disease-related processes in AD. Such findings would lay the foundation for larger clinical trials and could open the door to a new, multimodal approach to slowing or preventing Alzheimer's progression.
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