Summer 2026 Alzheimer’s Disease Update: New Blood Tests, Treatments, and Prevention Research

Anton Ostashko, MD·Last medically reviewed July 11, 2026

Overview

Alzheimer’s disease care is entering a new phase. Diagnosis still begins with a careful history, assessment of day-to-day function, neurological examination, cognitive testing, brain imaging, and evaluation for other causes of cognitive change. Biomarkers obtained through amyloid PET, cerebrospinal fluid (CSF), and increasingly blood testing can then help determine whether Alzheimer’s biology is present. Biomarker confirmation is especially important before disease-modifying anti-amyloid treatment.

In 2026, an estimated 7.4 million Americans age 65 and older are living with clinical Alzheimer’s dementia—about 1 in 9 people in this age group. The number is projected to approach 13 million by 2050.1

The most important Alzheimer’s updates as of July 11, 2026 are:

  • Two FDA-cleared blood biomarker tests now have defined clinical roles. The Lumipulse pTau217/β-amyloid 1-42 ratio is intended for specialized-care evaluation, while Elecsys pTau181 is primarily a rule-out test before specialty referral. Neither should be used for population screening or interpreted without a full clinical assessment.24
  • An FDA Class II recall affects specified Lumipulse reagent lots. Affected lots could produce falsely elevated ratios and excessive positive or indeterminate classifications. The FDA lists the cause as under investigation.3
  • Leqembi® and Kisunla™ remain the current FDA-approved disease-modifying anti-amyloid treatments for selected patients with mild cognitive impairment or mild dementia due to Alzheimer’s disease and confirmed amyloid pathology. Their average clinical effects are modest, and both require careful MRI-based safety monitoring.812
  • A subcutaneous Leqembi starting regimen remains investigational. Eisai and Biogen reported that the FDA extended its action date to August 24, 2026 after requesting additional information. The companies stated that no approvability concern had been raised to date, but this is a sponsor-reported update and not an FDA approval.10
  • Research is expanding beyond conventional anti-amyloid antibodies. Brain-shuttle delivery, tau-directed drugs, combination therapy, presymptomatic-treatment studies, and multidomain lifestyle interventions remain active areas of investigation. Promising biomarker results do not necessarily mean that a drug has been shown to preserve memory or daily function.

Evidence cutoff: This article reflects publicly available evidence through July 11, 2026. The main Alzheimer’s Association International Conference is scheduled for July 12–15, 2026 in London and online. Findings scheduled for presentation are described as pending rather than as established results.25

Understanding Alzheimer’s Disease

Alzheimer’s-related biological changes can begin many years before recognizable symptoms—sometimes up to 20 years before measurable cognitive impairment.1 The disease involves several interacting processes:

  • Amyloid plaques: Abnormal deposits of amyloid-beta protein outside brain cells. Amyloid can accumulate early, before substantial functional impairment is apparent.
  • Tau tangles: Abnormal tau protein inside neurons. The distribution and burden of tau generally track clinical severity more closely than amyloid burden, making tau an important therapeutic and prognostic research target.
  • Synaptic injury and neurodegeneration: Neuroinflammation, vascular injury, oxidative stress, impaired cellular clearance, and other mechanisms contribute to loss of synapses and brain cells. Alzheimer’s disease often coexists with vascular disease, Lewy body pathology, TDP-43 pathology, or other age-related brain changes.

Possible Early Symptoms

  • Repeatedly forgetting recent conversations, appointments, or events
  • Increasing difficulty managing finances, medications, planning, navigation, or familiar technology
  • Word-finding difficulty or reduced ability to follow complex conversations
  • Loss of efficiency or independence in activities that were previously routine

Depression, anxiety, apathy, irritability, and sleep disturbance can accompany early cognitive disorders, but these symptoms are nonspecific. By themselves, they do not establish Alzheimer’s disease and may point to a different or treatable condition.

Symptoms as the Disease Progresses

  • Memory loss that interferes with everyday activities
  • Difficulty solving problems or completing familiar tasks
  • Confusion about dates, locations, or situations
  • Language, visuospatial, or judgment difficulties
  • Behavioral or personality changes, including anxiety, suspicion, agitation, or apathy

How We Diagnose Alzheimer’s Disease in 2026

A modern Alzheimer’s evaluation is staged: first determine whether a progressive cognitive syndrome is present, then evaluate alternative or contributing causes, and finally assess whether Alzheimer’s biology explains the symptoms.

Initial Clinical Evaluation

  • A detailed history, including information from a knowledgeable family member or care partner when possible
  • Assessment of changes in work, finances, driving, medications, household tasks, and other daily activities
  • Neurological examination and office cognitive testing such as the MoCA or MMSE
  • Review of medications, alcohol or substance exposure, mood, sleep, hearing, vision, and vascular risk
  • Laboratory testing for potentially reversible or contributing problems, commonly including thyroid and vitamin B12 abnormalities when appropriate
  • Brain MRI, or CT when MRI is not feasible, to assess vascular injury, tumors, hydrocephalus, prior trauma, hemorrhage, and patterns of atrophy
  • Formal neuropsychological testing when detailed characterization, differential diagnosis, capacity assessment, or a reproducible baseline is needed

Blood-Based Biomarker Testing: Major 2025–2026 Developments

Blood biomarkers can make Alzheimer’s evaluation more accessible, but assays differ substantially in intended use, performance, cutoffs, and regulatory status. A result should be interpreted only in the population and clinical setting for which the test has been validated.

Lumipulse G pTau217/β-Amyloid 1-42 Plasma Ratio

The FDA cleared this test on May 16, 2025 for adults age 50 and older who have signs or symptoms of cognitive decline and are being evaluated in a specialized-care setting. A positive result means amyloid pathology is likely; it does not by itself establish a clinical diagnosis of Alzheimer’s disease. An indeterminate result requires additional evaluation, and every result must be interpreted together with the clinical assessment.2

⚠️ Important recall notice: The FDA posted a Class II recall affecting specified Lumipulse lots after reports that falsely elevated ratios produced excessive positive or indeterminate classifications and reduced specificity compared with amyloid PET or CSF. The FDA lists the cause as under investigation. Laboratories should not use affected lots, and clinicians should verify the reagent lot and reassess a prior result when it could change diagnosis or treatment.3

Elecsys pTau181

The FDA cleared Elecsys pTau181 on October 8, 2025 for the initial assessment of adults age 55 and older with cognitive complaints or symptoms, before referral to specialized care. Its main role is to help rule out amyloid pathology. In the 312-participant validation study, the negative predictive value was 97.9%, while the positive predictive value was 22.4% in a population with relatively low amyloid-PET prevalence. A positive result therefore does not diagnose Alzheimer’s disease and requires further evaluation.4

How Blood Results Should Be Used

The 2025 Alzheimer’s Association specialty-care guideline classifies blood biomarkers by their independently validated performance rather than treating every assay as interchangeable. A sufficiently sensitive test may be used for triage, in which a positive result is confirmed with amyloid PET or CSF. A higher-performing test that meets stringent sensitivity and specificity thresholds may, in some specialty-care settings, serve as a confirmatory biomarker instead of PET or CSF.5

Bottom line: Blood biomarkers should not be used for general-population screening and do not replace a comprehensive clinical evaluation. PET or CSF remains appropriate when a result is indeterminate, conflicts with the clinical picture, comes from an assay without adequate validation, or does not provide enough certainty for a high-stakes treatment decision. Coverage and out-of-pocket cost vary by assay, laboratory, Medicare contractor, and commercial insurer.

Imaging, CSF, and Genetic Risk Assessment

  • Amyloid PET remains an important way to confirm brain amyloid. In 2023, CMS removed the former national coverage-with-evidence-development restriction and allowed local Medicare contractors to make coverage decisions; access and patient cost still vary.6
  • Tau PET with TAUVID® can estimate the density and distribution of aggregated tau neurofibrillary tangles in adults with cognitive impairment who are being evaluated for Alzheimer’s disease. In selected specialty or research settings, it may provide staging or prognostic information. Tau PET is not required by the current U.S. Leqembi or Kisunla labels and is not established as a routine individual predictor of treatment response.7812
  • CSF biomarker testing remains a valid confirmatory option, particularly when blood results are unavailable, indeterminate, or discordant with the clinical picture.
  • Volumetric MRI software, such as NeuroQuant, can supplement expert visual MRI interpretation by quantifying regional brain volumes. Volumetric findings are not specific for Alzheimer’s disease and should not be used alone to establish the diagnosis.
  • APOE genotyping is recommended before anti-amyloid treatment to inform ARIA risk counseling. APOE ε4 carriers—especially people with two ε4 copies—have higher ARIA risk. Testing does not determine with certainty who will develop Alzheimer’s disease, and genetic counseling may be appropriate.812

Treatment and Management

Symptomatic Oral Therapies

  • Cholinesterase inhibitors—donepezil, rivastigmine, and galantamine—may provide modest symptomatic benefit for cognition or daily function in appropriate patients. Donepezil is taken once daily. When bedtime dosing causes vivid dreams, insomnia, or disrupted sleep, switching to morning dosing is a reasonable individualized adjustment.
  • Memantine is generally used in moderate-to-severe Alzheimer’s dementia and may be combined with a cholinesterase inhibitor.

These medications may help symptoms or function in some patients, but they have not been shown to remove amyloid or stop the underlying disease process.

Disease-Modifying Anti-Amyloid Therapy

Leqembi and Kisunla are intended for patients with mild cognitive impairment or mild dementia due to Alzheimer’s disease, the stages in which they were studied, and require confirmation of amyloid pathology before treatment. They have not been established for moderate or advanced dementia. Treatment selection also depends on MRI findings, bleeding risk, antithrombotic treatment, medical comorbidities, the ability to complete monitoring, and the patient’s goals.812

These medicines do not cure Alzheimer’s disease or restore lost memory. Their purpose is to reduce the average rate of cognitive and functional decline. The strongest causal evidence comes from the randomized trials; three- and four-year extension findings are clinically informative but less certain because the continuously randomized placebo comparisons had ended.

Leqembi® (Lecanemab)

  • How it is given: 10 mg/kg by IV infusion every two weeks for the first 18 months. The current U.S. label then permits continued every-two-week IV treatment, monthly IV maintenance, or 360 mg subcutaneous maintenance once weekly.8
  • MRI schedule: baseline MRI and surveillance MRIs before the 3rd, 5th, 7th, and 14th infusions, with additional imaging when symptoms or clinical circumstances warrant it.8
  • Randomized result: over 18 months, CDR-SB worsened by 1.21 points with lecanemab and 1.66 with placebo—an absolute difference of 0.45 point and 27% relative slowing.9
  • Four-year context: open-label-extension analyses using matched natural-history cohorts estimated approximately 11.0 to 13.1 months of time-equivalent slowing at 48 months. This means the average treated group reached a comparable measured level of worsening roughly a year later; it is not a guaranteed extra year without symptoms, and the long-term comparison was not randomized.1126

Kisunla™ (Donanemab)

  • How it is given: IV infusion every four weeks using the current modified titration of 350 mg, 700 mg, 1,050 mg, and then 1,400 mg from the fourth infusion onward.12
  • MRI schedule: baseline MRI and surveillance MRIs before the 2nd, 3rd, 4th, and 7th infusions, with additional imaging when clinically indicated.12
  • PET-based course completion: clinicians may consider stopping after amyloid PET confirms reduction to minimal plaque levels. In the pivotal program, 47% of treated participants met the trial’s PET completion criteria by 12 months and 69% by 18 months. Reaching a PET threshold is not the same as a cure or proof of clinical stability, and amyloid can reaccumulate.1227
  • Randomized result: over 76 weeks, CDR-SB worsened by 1.72 points with donanemab and 2.42 with placebo—an absolute difference of 0.70 point and approximately 29% relative slowing.13
  • Three-year context: the long-term extension reported 1.2 points less CDR-SB worsening versus a weighted ADNI external cohort and an estimated 6.9 months of time-equivalent slowing at three years. These findings support persistence of benefit but are not a continuation of randomized placebo-controlled follow-up.14

For the detailed benefit-risk discussion: our companion guide, Anti-Amyloid Infusion Therapy for Early Alzheimer’s Disease, explains ARIA-E and ARIA-H, APOE ε4 risk, genotype-specific numbers, MRI monitoring, infusion reactions, blood-thinner and stroke-treatment precautions, longer-term outcomes, and emergency symptoms. Keeping those details in the dedicated guide allows this general Alzheimer’s update to remain a broad overview.

A Balanced View of Anti-Amyloid Therapy in 2026

The pivotal lecanemab and donanemab trials demonstrated statistically significant slowing of decline, but the absolute differences were modest. Relative percentages such as 27% or 29% should always be presented alongside the underlying CDR-SB differences so that patients and families can judge the likely magnitude of benefit.

An April 2026 Cochrane review pooled 17 trials involving 20,342 participants across the anti-amyloid monoclonal-antibody class. The reviewers concluded that average cognitive and functional effects at approximately 18 months were absent or too small to be clinically important, while ARIA and bleeding-related harms increased.15 Others argue that a broad class-level analysis can obscure differences between older unsuccessful antibodies and newer plaque-clearing agents. The disagreement is not resolved simply by citing either relative percentages or a pooled class estimate.

The clearest way to explain the evidence to families is: these medications are not cures, do not restore lost memory, and may not produce a noticeable day-to-day difference for every patient. They can modestly reduce the average rate of decline in carefully selected people with early, amyloid-confirmed Alzheimer’s disease. Whether that potential benefit is worth the MRI surveillance, infusion or injection burden, ARIA and hemorrhage risk, uncertainty, and cost is an individualized decision.

Related guide: For a patient-level comparison of Leqembi and Kisunla—including exact ARIA and APOE risk tables—see Anti-Amyloid Infusion Therapy: Benefits, ARIA Risks, and Safety Monitoring.

Research Advances to Watch

Trontinemab: A Brain-Shuttle Anti-Amyloid Antibody

Trontinemab is designed to improve delivery of an anti-amyloid antibody across the blood-brain barrier using a transferrin-receptor brain shuttle. In company-reported Phase 1b/2a data, 91% of participants receiving the 3.6 mg/kg dose reached amyloid-PET negativity by 28 weeks, while ARIA-E was reported in fewer than 5% across the 1.8 and 3.6 mg/kg cohorts.16

These are encouraging biomarker and early safety findings, not evidence yet that trontinemab slows cognitive or functional decline. Phase 3 TRONTIER studies are underway, including an approximately 800-participant early symptomatic Alzheimer’s study with estimated primary completion in 2028.17

Tau-Directed Therapies: Important Questions Remain

Tau is an attractive target because tau burden and distribution are closely associated with neurodegeneration and clinical severity. However, no tau-directed drug has yet demonstrated confirmatory Phase 3 clinical efficacy in Alzheimer’s disease.

  • Posdinemab: Johnson & Johnson reported that the Phase 2b Auτonomy proof-of-concept study did not show statistically significant slowing of clinical decline, and the Alzheimer’s program was discontinued.18
  • Bepranemab: The Phase 2a TOGETHER trial did not meet its primary CDR-SB endpoint in the overall population. Secondary cognitive, tau-PET, and predefined subgroup findings were exploratory and require confirmation rather than being treated as established clinical efficacy.19
  • Etalanetug (E2814): A very small early study in dominantly inherited Alzheimer’s disease showed substantial reductions in CSF MTBR-tau biomarkers and signals of tau-PET stabilization. These findings demonstrate biological target engagement, not proven cognitive benefit. Combination studies with lecanemab are ongoing.20
  • Diranersen (BIIB080): These are two names for the same tau-lowering antisense oligonucleotide. Biogen reported in May 2026 that the Phase 2 CELIA study did not meet its prespecified primary dose-response CDR-SB endpoint at week 76. Sponsor-reported biomarker, secondary, and exposure-response findings are preliminary pending full presentation and peer review.21

Presymptomatic Treatment and Risk-Reduction Trials

  • AHEAD 3-45: Lecanemab in cognitively unimpaired adults with intermediate or elevated amyloid.
  • TRAILBLAZER-ALZ 3: Donanemab in cognitively unimpaired adults with preclinical Alzheimer’s disease.
  • Tau NexGen and other combination studies: Sequential or concurrent anti-amyloid and anti-tau treatment, including studies in autosomal-dominant Alzheimer’s disease.20
  • PrevenTRON: A planned trontinemab program in preclinical Alzheimer’s disease.16

Positive results would support presymptomatic treatment or delayed symptom onset; they would not automatically prove that Alzheimer’s disease had been permanently prevented. These studies are ongoing, and treatment of asymptomatic people is not routine clinical care outside an appropriate research protocol.22

Lifestyle: What U.S. POINTER Showed

The 2,111-participant U.S. POINTER randomized trial compared a structured two-year multidomain program with a self-guided program in older adults at increased risk for cognitive decline. Both groups improved on a global cognitive composite, and the structured program produced a modestly greater improvement. The trial supports structured attention to exercise, nutrition, cardiovascular risk, cognitive and social engagement, but it did not establish that the intervention prevents Alzheimer’s disease or dementia.23

Practical brain-health care still includes regular physical activity, treatment of hypertension and diabetes, smoking cessation, sleep evaluation, identification and treatment of hearing loss, medication review, adequate nutrition, fall prevention, and meaningful cognitive and social activity.

A Notable Negative Result: Semaglutide

In the Phase 3 EVOKE and EVOKE+ randomized trials, oral semaglutide did not significantly slow clinical progression in early symptomatic Alzheimer’s disease. The peer-reviewed 2026 results are a useful reminder that associations seen in observational datasets do not establish that a metabolic medication treats Alzheimer’s disease.24

Conditions That Can Look Like Alzheimer’s Disease

Before committing to an Alzheimer’s diagnosis—or to Alzheimer’s-directed treatment—it is essential to consider other explanations and coexisting conditions:

  • Potentially reversible or partly reversible contributors: thyroid disease, vitamin B12 deficiency, sleep apnea, depression, medication effects, alcohol or substance exposure, hearing loss, and visual impairment
  • Vascular cognitive impairment and prior strokes
  • Lewy body disease and Parkinson’s disease dementia
  • Frontotemporal dementia
  • LATE/TDP-43 pathology, which often coexists with Alzheimer’s pathology in older adults
  • Normal-pressure hydrocephalus
  • Cerebral amyloid angiopathy, which is particularly relevant to hemorrhage and ARIA risk
  • Seizure disorders, autoimmune or inflammatory disease, cancer, infection, toxic exposure, or other neurological disorders when suggested by the history or examination

These distinctions change prognosis, treatment choices, medication safety, and eligibility for anti-amyloid therapy.

The Best Alzheimer’s Care in 2026 Is Staged and Individualized

  1. Confirm the syndrome. Determine whether there is objective, progressive cognitive impairment and how it affects daily function.
  2. Identify contributing and alternative causes. Review sleep, mood, medications, hearing, vascular risk, laboratory findings, and structural brain imaging rather than assuming every memory concern is Alzheimer’s disease.
  3. Confirm the biology when it will change care. Use a validated blood biomarker, amyloid PET, or CSF testing in the appropriate clinical setting. Tau PET may answer selected staging or prognostic questions but is not routinely required.
  4. Confirm the treatment window and safety profile. Anti-amyloid treatment is limited to early symptomatic, amyloid-confirmed disease. Review MRI findings, APOE genotype, antithrombotic therapy, bleeding risk, comorbidities, logistics, and patient goals.
  5. Combine medication decisions with comprehensive care. Address physical activity, vascular health, sleep, hearing, nutrition, medication burden, driving and home safety, caregiver support, legal and financial planning, and advance care planning.

Bottom line: Alzheimer’s care is improving, but the field remains early. We can now characterize disease biology more accurately and offer disease-modifying treatment to selected patients at an early stage. The next advances may come from better-validated blood tests, safer delivery systems, tau and combination strategies, and effective presymptomatic treatment—but each must be judged by demonstrated cognitive and functional outcomes, not biomarker change alone.

At Los Altos Neurology, we provide individualized cognitive evaluation, interpretation of plasma biomarkers with appropriate confirmatory follow-up, assessment for Leqembi and Kisunla eligibility, shared decision-making, and coordinated safety monitoring. The goal is not simply to order the newest test or medication, but to determine which findings and treatments are medically appropriate for each patient.

References

  1. Alzheimer’s Association. 2026 Alzheimer’s Disease Facts and Figures. Alzheimer’s & Dementia. 2026;22. doi:10.1002/alz.71345.
  2. U.S. Food and Drug Administration. Lumipulse G pTau 217/β-Amyloid 1-42 Plasma Ratio: 510(k) Decision Summary (K242706). May 16, 2025.
  3. U.S. Food and Drug Administration. Class II Device Recall: Lumipulse G pTau 217/β-Amyloid 1-42 Plasma Ratio. Recall initiated December 11, 2025; FDA posting February 5, 2026.
  4. U.S. Food and Drug Administration. Elecsys pTau181: 510(k) Decision Summary (K252163). October 8, 2025.
  5. Palmqvist S, et al. Alzheimer’s Association clinical practice guideline on the use of blood-based biomarkers in the diagnostic workup of suspected Alzheimer’s disease within specialized care settings. Alzheimer’s & Dementia. 2025;21:e70535. doi:10.1002/alz.70535.
  6. Centers for Medicare & Medicaid Services. National Coverage Analysis Decision Memo: Beta Amyloid Positron Emission Tomography in Dementia and Neurodegenerative Disease. October 13, 2023.
  7. U.S. Food and Drug Administration. TAUVID (flortaucipir F 18) Prescribing Information. 2024.
  8. U.S. National Library of Medicine. LEQEMBI (lecanemab-irmb) U.S. Prescribing Information. Label updated June 30, 2026; accessed July 11, 2026.
  9. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in Early Alzheimer’s Disease. N Engl J Med. 2023;388:9-21. doi:10.1056/NEJMoa2212948.
  10. Eisai Co., Ltd. and Biogen Inc. Update on FDA Priority Review of LEQEMBI IQLIK Subcutaneous Injection as a Starting Dose for Early Alzheimer’s Disease. May 8, 2026. Sponsor news release.
  11. Eisai Co., Ltd. and Biogen Inc. Four-year open-label-extension analyses of lecanemab presented at AAIC 2025. July 31, 2025. Sponsor news release.
  12. U.S. National Library of Medicine. KISUNLA (donanemab-azbt) U.S. Prescribing Information. Current label accessed July 11, 2026.
  13. Sims JR, Zimmer JA, Evans CD, et al. Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial. JAMA. 2023;330(6):512-527. doi:10.1001/jama.2023.13239.
  14. Zimmer JA, Sims JR, Evans CD, et al. Donanemab in early symptomatic Alzheimer’s disease: results from the TRAILBLAZER-ALZ 2 long-term extension. J Prev Alzheimers Dis. 2026;13(2):100446. doi:10.1016/j.tjpad.2025.100446.
  15. Nonino F, et al. Amyloid-beta-targeting monoclonal antibodies for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease. Cochrane Database Syst Rev. 2026;4:CD016297. doi:10.1002/14651858.CD016297.
  16. F. Hoffmann-La Roche Ltd. Phase 1b/2a trontinemab biomarker and safety findings presented at AAIC 2025. July 28, 2025. Sponsor news release.
  17. ClinicalTrials.gov. Phase 3 Study of Trontinemab in Participants With Early Symptomatic Alzheimer’s Disease (NCT07169578). Accessed July 11, 2026.
  18. Johnson & Johnson. Statement on the Auτonomy study of posdinemab. November 21, 2025. Sponsor statement.
  19. UCB. Phase 2a TOGETHER study results for bepranemab. October 31, 2024. Sponsor news release.
  20. Eisai Co., Ltd. Early etalanetug (E2814) biomarker findings presented at CTAD 2025. December 2, 2025. Sponsor news release.
  21. Biogen Inc. Topline Results from the Phase 2 CELIA Study of Diranersen (BIIB080). May 14, 2026. Sponsor news release.
  22. ClinicalTrials.gov. AHEAD 3-45 (NCT04468659); and TRAILBLAZER-ALZ 3 (NCT05026866). Accessed July 11, 2026.
  23. Baker LD, et al. Structured vs Self-Guided Multidomain Lifestyle Interventions for Global Cognitive Function: The U.S. POINTER Randomized Clinical Trial. JAMA. 2025;334(8):681-691. doi:10.1001/jama.2025.12923.
  24. Cummings JL, Atri A, Sano M, et al. Efficacy and safety of oral semaglutide 14 mg in early-stage symptomatic Alzheimer’s disease (evoke and evoke+): two Phase 3 randomized, placebo-controlled trials. The Lancet. Published online March 19, 2026. doi:10.1016/S0140-6736(26)00459-9.
  25. Alzheimer’s Association. Alzheimer’s Association International Conference 2026. July 12-15, 2026, London and online.
  26. Dickson S, Whetten J, Hendrix S, et al. Long-Term Benefit of Lecanemab: Estimation of Time Saved Through 48 Months. CTAD 2025 poster. Sponsor-supported conference material.
  27. Eli Lilly and Company. KISUNLA efficacy and treatment-completion data. HCP website summarizing TRAILBLAZER-ALZ 2 and long-term analyses; accessed July 11, 2026.

Medical disclaimer. This article is provided for general educational and informational purposes only. It does not constitute individualized medical advice, diagnosis, treatment, a recommendation for any specific test or therapy, or informed consent. Medical information changes over time, and this article may not reflect developments occurring after its stated review date or apply to your individual circumstances. Do not disregard or delay professional medical advice, or start, stop, or change any medication or treatment, based on this article. Discuss personal medical decisions with a qualified healthcare professional who can evaluate your individual history and circumstances. Accessing or using this website does not, by itself, create a physician–patient relationship with Los Altos Neurology or any of its clinicians. Do not use this website for urgent or emergency medical concerns; call 911 or seek immediate emergency care. Although Los Altos Neurology makes reasonable efforts to provide accurate and current information, it does not guarantee that all content is complete, current, or applicable to every individual. See our full Medical Disclaimer.