Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators.
Why it matters
This study found differences in inflammatory lipid molecules in both brain and liver tissue from people who had Alzheimer's disease compared to those who did not. The liver showed more widespread changes, suggesting it may play a role in the body-wide inflammation seen in Alzheimer's, but this is tissue analysis and does not test treatments.
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INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia.
Why it matters
This study of brain tissue found that different types of dementia neuropathology are driven by distinct genetic variants but converge on shared genes and biological processes. It is genetic research that may inform understanding of mixed dementia but does not test any treatment.
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While normalizing biomarker values by A{beta}40 or A{beta}42 reduced physiological variability for some biomarkers, the effects of the normalization were compartment-, and cohort-dependent.
Why it matters
This analysis explains when and why normalizing Alzheimer's biomarker values by dividing them by another biomarker is likely to improve their usefulness. It is methodological work to strengthen biomarker interpretation in trials, not a study of any treatment or prevention.
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INTRODUCTIONMultimodal lifestyle interventions can delay or slow Alzheimers disease (AD) in at-risk older adults, and plasma pTau217, a blood-based biomarker, now enables scalable AD risk stratification.
Why it matters
This pilot study screened older adults for Alzheimer's risk using genetics and a blood biomarker, then gave high-risk participants a six-month lifestyle coaching program. It is a small pilot focused on feasibility and attitudes toward risk disclosure, and it does not show whether the intervention prevents Alzheimer's disease.
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Structured AbstractO_ST_ABSBackgroundC_ST_ABSThe genetic architecture of Alzheimer disease remains incompletely understood.
Why it matters
This study in Midwestern Amish communities found that common genetic variants explain much of Alzheimer's risk in APOE-e4 carriers, while other factors remain unexplained in non-carriers, and identified RIN3 and PILRA as linked to cognitive impairment risk. It is genetic research that may guide future work but does not offer a treatment or cure.
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Structured AbstractO_ST_ABSINTRODUCTIONC_ST_ABSThe Collaborative Amish Aging and Memory Project (CAAMP) is an ongoing longitudinal study spanning multiple sites, focused on cognitive function and age-related traits in Midwestern Amish (Ohio and Indiana) communities.
Why it matters
This describes an ongoing long-term study of nearly 4,000 Amish participants that collects clinical, genetic, and biomarker data to study cognitive aging and Alzheimer's disease. It is a resource for future research and reports no results yet on treating, curing, or preventing the disease.
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Alzheimers disease and related dementias (ADRD)1 and Parkinsons disease and related disorders (PDRD)2 have substantial genetic contributions, yet the role of rare damaging coding variants remains incompletely characterized at population scale3-6.
Why it matters
This large genetic study confirmed known risk genes and identified new ones, including IMPA2 for Alzheimer's disease and related dementias. It adds to understanding of the genetic causes of these diseases but does not test any treatment or prevention.
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INTRODUCTIONDetermining whether plasma biomarkers are preferentially associated with Alzheimers disease (AD)-related rather than age-related brain atrophy patterns may clarify their prognostic and diagnostic clinical use.
Why it matters
This study found that several blood biomarkers were linked to later development of MCI or dementia due to Alzheimer's disease, and to changes in brain atrophy patterns over time. It is observational research on biomarkers for diagnosis and prognosis, not a test of any treatment or cure.
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ObjectiveTo externally replicate and extend prior findings across two structurally independent healthcare data sources, evaluating whether predominant use of antihypertensive medications that stimulate versus inhibit angiotensin II type 2 and type 4 receptor signaling is associated with risk of incident ADRD.
Why it matters
Across two large healthcare databases, people who mainly took blood pressure medications that stimulate certain angiotensin receptors had a modestly lower risk of developing Alzheimer's disease and related dementias than those taking inhibiting types. This is observational evidence only, and the authors say randomized trials are needed before any treatment recommendations can be made.
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INTRODUCTIONSleep-dependent memory consolidation is impaired early in Alzheimers disease (AD).
Why it matters
In a small randomized trial of 37 patients with early Alzheimer's disease, one night of closed-loop auditory stimulation during sleep improved overnight memory consolidation compared with sham stimulation. The authors note that further studies are needed to see whether these effects last with multiple nights of treatment.
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ImportanceAnxiety phenotypes - rumination, global anxiety, and worry (RAW) - are increasingly associated with Alzheimers disease and related dementias (ADRD) risk, yet how anxiety phenotypes relate to coordinated, multi-system biology in the at-risk older adults is unknown.
Why it matters
In 110 older adults without dementia, anxiety-related traits such as rumination and worry were linked to a pattern of blood proteins related to neurodegeneration. This is cross-sectional observational research and does not show whether treating anxiety would reduce dementia risk.
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Plasma biomarkers of amyloid-associated tau phosphorylation (T1) and established tau proteinopathy (T2) can approximate Alzheimers disease stage, but whether plasma-defined stages correspond to broader biological states is unknown.
Why it matters
This study used plasma proteomics to define five stages of Alzheimer's disease that mapped onto distinct biological states and ordered clinical trajectories. It is about staging and understanding disease biology, not about treating, curing, or preventing Alzheimer's disease.
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BackgroundNon-pharmacological interventions may enhance motor-cognitive integration in prodromal Alzheimers disease (pAD).
Why it matters
In this 12-month pilot randomized trial, a partnered rhythmic rehabilitation dance intervention met feasibility and safety criteria but showed no significant group-by-time interaction for the primary motor outcome compared with group walking. It is a small pilot study of a non-pharmacological intervention, not a treatment, cure, or prevention for Alzheimer's disease.
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BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases.
Why it matters
This study found that clonal haematopoiesis was associated with a progressive, left-lateralised cortical atrophy pattern that resembles Alzheimer's disease signatures in cognitively healthy older adults. It suggests clonal haematopoiesis may mark biological processes linked to brain atrophy, but it is not a treatment, cure, or prevention.
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BackgroundAnti-amyloid-{beta} (A{beta}) monoclonal antibodies are disease-modifying treatments for early Alzheimers disease but are associated with amyloid-related imaging abnormalities (ARIA) and intracranial hemorrhage (ICH).
Why it matters
This analysis of adverse event reports found potential drug-drug interaction signals between anti-amyloid-β antibodies and antithrombotic drugs for amyloid-related imaging abnormalities and intracranial hemorrhage. It suggests caution with aspirin and thrombolysis during antibody treatment, but prospective validation is needed and it is not about curing or preventing Alzheimer's disease.
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INTRODUCTIONIndividuals with Alzheimers disease (AD) exhibit substantial heterogeneity in the severity of vascular changes and neurodegeneration, making the identification of biologically meaningful subtypes across the AD spectrum critical for improving prognosis and tailoring interventions.
Why it matters
This multicohort study identified two data-driven subtypes of Alzheimer's disease based on MRI: one with early atrophy and one with initially elevated white matter hyperintensity volumes. The atrophy-first subtype had a higher risk of conversion to Alzheimer's disease, but this is about subtyping and prognosis, not treatment, cure, or prevention.
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BackgroundDementia is rising worldwide, and in Alzheimer Disease (AD) the loss of communication adds to the burden.
Why it matters
In this small pilot study, 20 people with Alzheimer's disease learned to make a video call through errorless learning, with verbal errors falling and motor errors increasing. It is an early, preliminary study about learning a daily task, not about treating, curing, or preventing Alzheimer's disease.
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Brain iron accumulation is well established in Alzheimers disease (AD), but whether the two share a genetic basis remains unclear.
Why it matters
This genetic study found that brain iron deposition and Alzheimer's disease share a polygenic basis, especially in basal ganglia structures. It identifies shared genetic factors but does not test any treatment, cure, or prevention.
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BackgroundAlzheimers disease (AD) pathology often accumulates years before memory loss, creating a need to identify high-risk individuals presymptomatically.
Why it matters
This study found that people with extreme high polygenic risk scores were more likely to have Alzheimer's disease across ancestries, including some without the APOE ε4 variant. It is about identifying high-risk individuals, not about treating, curing, or preventing the disease.
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We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa
Why it matters
This observational cohort study used data from 14,364 All of Us Research Program participants with type 2 diabetes to examine whether educational attainment and Alzheimer disease genetic risk were associated with GLP-1 receptor agonist initiation and dementia incidence. It compared GLP-1 receptor agonist initiators with initiators of other second-line therapies to assess the estimated association with incident dementia.
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IntroductionPolygenic risk scores (PRS) may improve Alzheimers disease (AD) risk prediction before symptom onset, yet choosing an appropriate model can be challenging.
Why it matters
This study evaluated 1,752 polygenic risk score models and found results were not consistent across methods, with most individuals falling in both the top and bottom risk deciles depending on the model. It concerns genetic risk prediction methods and does not test any treatment, cure or prevention.
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Alzheimers disease (AD) is characterized by substantial clinical and biological heterogeneity, with diverse neuroanatomical, cognitive, clinical, functional, and genetic risk profiles that are poorly captured by current diagnostic frameworks.
Why it matters
This study identified two MRI-based neuroanatomical dimensions of Alzheimer's disease, one with widespread atrophy and more severe cognitive, clinical and functional impairment and higher genetic risk, and one with relatively preserved brain patterns. It describes disease heterogeneity and does not test any treatment, cure or prevention.
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INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations.
Why it matters
This study found that the APOE e4 effect on pTau217 was about 2.5-fold larger in participants of European-like ancestry than African-like ancestry, and that African ancestry weakened these associations. It concerns how genetic ancestry affects biomarker interpretation and does not test any treatment, cure or prevention.
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INTRODUCTIONMultimodal biomarkers have transformed Alzheimers disease research, but the incremental contribution of each modality to predicting progression from mild cognitive impairment (MCI) remains unclear.
Why it matters
This study compared how much each type of biomarker adds to predicting progression from mild cognitive impairment to Alzheimer's over 24 months, and found that removing cognitive assessments caused the largest drop in performance. It is about prediction modeling and does not test any treatment, cure or prevention.
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BackgroundAccurate prediction of progression from mild cognitive impairment (MCI) to Alzheimers disease (AD) is important for prognosis, patient management, and clinical trial enrollment.
Why it matters
This study found that episodic memory and functional assessment were the strongest individual predictors of 24-month progression from mild cognitive impairment to Alzheimer's, and that combining episodic memory, functional assessment and executive function performed best. It is about prediction and does not test any treatment, cure or prevention.
From across this topic
10 of the 5,374 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.
- Amyloid β-peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression
- Diagnostic performance of MK and Flortaucipir tau PET for the biological staging of Alzheimer disease
- MRI-derived brain aging trajectories across the Alzheimer's continuum: links to cognition, pathology and lifestyle risk factors
- Descobertas e avanços do sequenciamento de próxima geração na doença de Alzheimer
- Mitochondrial dysfunction, oxidative stress, neuroinflammation, and metabolic alterations in the progression of Alzheimer's disease: A meta-analysis of in vivo magnetic resonance spectroscopy studies
- The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study
- The clinical introduction of genetic testing for Alzheimer disease. An ethical perspective
- Diagnostic Performance of the α-Synuclein Seed Amplification Assay for Dementia With Lewy Bodies: A Comparison Across 4 Laboratories
- The Revised National Alzheimer's Coordinating Center's Neuropathology Form-Available Data and New Analyses
- Benchmarking machine learning models for late-onset alzheimer's disease prediction from genomic data