Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Alzheimer disease (AD) pathology begins 15–20 years before clinical symptoms, necessitating non - invasive biomarkers for early diagnosis.
Why it matters
This retrospective study of 400 participants developed a multimodal model combining neuron-derived exosome markers, plasma free biomarkers and imaging indicators for preclinical Alzheimer diagnosis. It is aimed at earlier diagnosis, not at treating, curing or preventing the disease.
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Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217.
Why it matters
Using 972 cerebrospinal fluid samples from 484 participants in the Dominantly Inherited Alzheimer Disease Network, this study found that core Alzheimer's disease biomarker abnormalities precede inflammatory and glial markers in autosomal dominant Alzheimer's disease. It clarifies the order of biomarker changes and does not test treatment, cure, or prevention.
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Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability.
Why it matters
This study presents a computer model predicting Alzheimer's disease progression across general, Down syndrome-associated, and autosomal dominant cohorts, with prediction accuracy varying by dataset. It is a prediction tool and does not treat, cure, or prevent the disease.
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16/100
Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E).
Why it matters
This cross-sectional study examined how different anti-amyloid antibodies bind to Aβ aggregates from human Alzheimer disease brain, noting that lecanemab is hypothesized to bind protofibrils that are not well-characterized in human brain. It states that it is unknown how binding differences correlate with ARIA-E rates and how the APOE ε4 allele, which increases ARIA-E risk, affects antibody binding.
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Researchers tested whether a tablet-based cognitive test (TabCAT) could substitute for traditional paper-and-pencil memory tests in people with early-onset Alzheimer's. Scores on the tablet's attention/executive tasks correlated strongly (above 0.7) with standard tests like the MMSE and MoCA, and one subtest could distinguish people with amyloid plaques from those without with good accuracy (AUC 0.82).
Why it matters
Researchers tested whether a tablet-based cognitive test could substitute for traditional paper-and-pencil memory tests in people with early-onset Alzheimer's and found that scores on the tablet's attention/executive tasks correlated strongly with standard tests like the MMSE and MoCA. One subtest could distinguish people with amyloid plaques from those without with good accuracy, supporting use of quicker digital tools for early detection.
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Trontinemab is designed with a molecular 'shuttle' that helps it cross into the brain more efficiently than older anti-amyloid antibodies, aiming for faster plaque removal at lower doses.
Why it matters
Trontinemab is designed with a molecular 'shuttle' that helps it cross into the brain more efficiently than older anti-amyloid antibodies, aiming for faster plaque removal at lower doses. In this early trial, the highest dose group saw a large drop in brain amyloid (over 100 centiloids on average) within about 7 months, along with meaningful drops in tau and neurodegeneration markers in spinal fluid.
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Mivelsiran takes a completely different approach from antibody drugs: it's injected into the spinal fluid and uses RNA interference to tell brain cells to make less of the amyloid precursor protein in the first place, rather than clearing plaques after they form.
Why it matters
Mivelsiran takes a completely different approach from antibody drugs: it's injected into the spinal fluid and uses RNA interference to tell brain cells to make less of the amyloid precursor protein in the first place, rather than clearing plaques after they form. In this early safety trial, a single dose cut a marker of amyloid production by over 80% within a month, and repeat dosing kept levels suppressed, with only mild-to-moderate side effects reported so far.
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The Phase 2a TOGETHER trial tested bepranemab, an antibody targeting the tau protein (rather than amyloid), in 466 people with prodromal-to-mild Alzheimer's disease over 80 weeks.
Why it matters
In the Phase 2a TOGETHER trial, the anti-tau antibody bepranemab did not improve the main cognitive/functional measure compared with placebo across the whole group, but it slowed tau buildup on PET scans by 33-58% overall. This is a Phase 2a trial, and the clinical endpoint was not met in the overall population.
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Blood-based biomarkers for Alzheimer’s disease (AD) have been widely studied, but direct comparisons of several biomarkers in clinical settings remain limited.
Why it matters
In this cross-sectional memory clinic study, plasma p-tau biomarkers had greater diagnostic performance and larger effect sizes than t-tau and Aβ42/40 assays for detecting biologically defined Alzheimer's disease. It is about diagnosis only and says nothing about treating, curing or preventing the disease.
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In September 2024 the SEC announced that Cassava Sciences and three individuals tied to the company agreed to pay over $40 million combined to settle federal charges that they misled investors about a 2020 Phase 2 trial of simufilam.
Why it matters
The SEC alleged that Cassava Sciences falsely claimed its 2020 Phase 2 simufilam trial was properly blinded and touted a large cognitive-memory improvement, when the full unblinded dataset showed no measurable improvement in episodic memory. The company and three individuals settled for over $40 million combined without admitting or denying the allegations.
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Adults with Down syndrome (DS) are at risk for Alzheimer’s disease (AD).
Why it matters
This cohort study of 167 adults with Down syndrome examined the timeline to symptomatic Alzheimer's disease based on estimated years since reaching amyloid positivity and in relation to tau. It describes biomarker timing only and tests no treatment or prevention.
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Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer.
Why it matters
This theoretical work used virtual screening and docking to explore interactions between small natural molecules and the KIBRA protein, a biomarker for synaptic dysfunction and cognitive decline, finding Hypericin had the lowest binding energy of approximately -9 kcal/mol. It notes that amyloid-targeting monoclonal antibodies such as lecanemab, aducanumab and donanemab remain controversial due to limited clinical benefits and significant side effects.
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By age 40 years over 90% of adults with Down syndrome (DS) have Alzheimer’s disease (AD) pathology and most progress to dementia.
Why it matters
This cross-sectional analysis examined how small vessel cerebrovascular disease relates to Alzheimer's-related brain changes and neurodegeneration in adults with Down syndrome. It suggests cerebrovascular disease may contribute to Alzheimer's processes in this group, but as an observational study it does not test any treatment or prevention.
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Arthritis includes approximately 100 conditions that affect the joints and surrounding tissues.
Why it matters
This report found that 55.9% of U.S. adults with dementia also had diagnosed arthritis, and about half of adults aged 65 or older with dementia also had arthritis. It describes prevalence of arthritis alongside dementia and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Recently-developed blood markers for Alzheimer’s (AD) detection have high accuracy but usually require ultra-sensitive analytic tools not commonly available in clinical laboratories.
Why it matters
This study tested blood markers for Alzheimer's disease on an automated lab platform in 367 people, including some with Down syndrome. It shows these blood tests can be run on standard equipment, but the text does not report how well they performed or any treatment implications.
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An independent US drug-pricing watchdog analyzed how lecanemab's actual price compares to its clinical benefit.
Why it matters
An independent US drug-pricing watchdog concluded that lecanemab would need to cost roughly $8,900 to $21,500 per year to be considered good value for money, well below its actual launch price of $26,500 per year. An expert committee also voted that, based on the trial evidence available at the time, lecanemab represented low long-term value at its current price.
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16/100
Eli Lilly's newer anti-amyloid antibody remternetug showed fast, dose-dependent removal of amyloid plaques in a small early trial: three-quarters of people getting the higher doses had their brain amyloid drop below the threshold used to call a scan 'positive' within about six months.
Why it matters
Eli Lilly's newer anti-amyloid antibody remternetug showed fast, dose-dependent removal of amyloid plaques in a small early trial: three-quarters of people getting the higher doses had their brain amyloid drop below the threshold used to call a scan 'positive' within about six months. Brain-swelling side effects (ARIA) occurred in about a quarter of participants, similar to other approved anti-amyloid drugs, with one symptomatic case.
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The author panel systematically reviewed available clinical trial data detailing aducanumab use in individuals with early symptomatic Alzheimer disease.
Why it matters
This report systematically reviewed clinical trial data on aducanumab use in individuals with early symptomatic Alzheimer's disease and assigned levels of evidence. It evaluates the strength of evidence for the drug's use rather than reporting a cure or prevention.
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Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk.
Why it matters
This work compared proteins in brain, cerebrospinal fluid, and plasma from people with sporadic and genetically defined Alzheimer's disease, and found a cerebrospinal fluid protein signature that distinguished cases with an area under the curve of 0.89 in the discovery group. It is a biomarker study, so it may help identify disease signatures but does not by itself show a way to treat, cure, or prevent Alzheimer's disease.
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Accelerated approval of aducanumab for mild Alzheimer's by the U.S. Food and Drug Administration on June 7, 2021, has generated substantial medical, scientific, and ethical controversy.
Why it matters
This article argues that aducanumab's accelerated approval was contrary to the FDA Advisory Committee's judgment that little reliable evidence existed of significant benefit, and it raises concerns about cost, side effects, and false hope. It is a commentary on approval and reimbursement, not new evidence that the drug treats or cures Alzheimer's disease.
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On June 7, 2021, the FDA granted accelerated approval to aducanumab (Aduhelm), the first new Alzheimer's drug approved since 2003 and the first ever approved for a mechanism thought to modify disease course.
Why it matters
Aducanumab received accelerated approval based only on its ability to reduce amyloid plaques on brain scans, not on proven cognitive benefit, and continued approval required a confirmatory trial. The decision was highly controversial, with an FDA advisory committee voting against approval and two committee members resigning afterward.
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OASIS-3 is a compilation of MRI and PET imaging and related clinical data for 1098 participants who were collected across several ongoing studies in the Washington University Knight Alzheimer Disease Research Center over the course of 15 years.
Why it matters
OASIS-3 brings together MRI, PET and clinical data on 1,098 people aged 42 to 95 (605 cognitively normal, 493 at various stages of cognitive decline), collected over 15 years across several studies at Washington University's Knight Alzheimer Disease Research Center. It includes more than 2,000 MRI sessions, more than 1,500 amyloid and metabolic PET scans, and ready-processed measurements such as brain-volume segmentations. It is a shared research resource, not a test of any treatment, and on its own it does not show what causes or changes Alzheimer's.
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Although large numbers of microRNAs (miRNAs) expressed in Alzheimer disease (AD) have been detected, their functions and mechanisms of regulation remain to be fully clarified.
Why it matters
This work found that miR-124 levels decrease in Alzheimer's disease and that miR-124 suppresses BACE1 expression by targeting Bace1 mRNA in vitro. This is laboratory work on a possible mechanism and does not establish a treatment for patients.
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Alzheimer's disease (Alzheimer's), an ultimately fatal form of dementia, is the sixth leading cause of death in the United States, accounting for 3.6% of all deaths in 2014 (1,2).
Why it matters
US Alzheimer's deaths rose 54.5% between 1999 and 2014, and more people died at home rather than in medical facilities. The report notes this likely added to the burden on unpaid caregivers, who might benefit from support interventions.
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Alzheimer’s disease (AD) is the most commonly occurring form of dementia.
Why it matters
This systematic review and economic model updated guidance on the clinical effectiveness and cost-effectiveness of donepezil, galantamine, rivastigmine and memantine for Alzheimer's disease. It reviews existing treatments for symptoms and does not report a cure or way to prevent the disease.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Finding Treatment Effects in Alzheimer Trials in the Face of Disease Progression Heterogeneity
- Neurofilament Light Predicts Decline in Attention but Not Episodic Memory in Preclinical Alzheimer's Disease
- Plasma Aβ42/40 Ratio Detects Early Stages of Alzheimer's Disease and Correlates with CSF and Neuroimaging Biomarkers in the AB255 Study
- Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways
- Avanços na doença de Alzheimer: diagnóstico precoce, biomarcadores e perspectivas futuras
- Stage-specific prevalence of behavioral symptoms in Alzheimer's disease in a multi-ethnic community sample
- Mutaciones en los genes PSEN1 y PSEN2 como marcadores moleculares en la Enfermedad de Alzheimer. Revisión Sistemática
- Accumulation of tumor-suppressor PTEN in Alzheimer neurofibrillary tangles
- Alzheimer's disease neurodegenerative biomarkers are associated with decreased cognitive function but not β-amyloid in cognitively normal older individuals
- Amyloid-PET pipeline choice influences classification of preclinical Alzheimers disease