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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Early identification of Alzheimers disease and related dementias (ADRD) remains challenging despite its importance for timely intervention, management of modifiable risk factors, and care planning.
Why it matters
This study compared models for predicting Alzheimer's disease and related dementias from electronic health records and found that simple count-based models performed best overall, with performance declining at longer prediction horizons. It is about risk prediction methods and does not test any treatment, cure or prevention.
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BackgroundPlasma phosphorylated tau at threonine 217 (p-Tau217) is a leading blood-based biomarker for Alzheimers disease (AD).
Why it matters
This study validated an automated blood test for p-Tau217 and assessed how well it distinguished PET-defined amyloid status in people with mild cognitive impairment or mild Alzheimer's dementia. It is a laboratory test evaluation and does not test any treatment, cure or prevention.
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BackgroundThe Centiloid (CL) scale standardizes global amyloid PET quantification and is widely used to define amyloid positivity.
Why it matters
This study developed a nine-region amyloid PET score that predicted cognitive decline more strongly than the Centiloid scale in ADNI and performed consistently in external validation cohorts. It is a prognostic imaging tool, not a treatment or cure.
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BackgroundFluid biomarkers enable the demonstration of the biological effects of novel therapies in Alzheimers disease (AD).
Why it matters
Using placebo-arm data from a phase 2b trial, this study described longitudinal fluid biomarker trajectories in early Alzheimer's disease and estimated sample sizes needed for trials, finding that heterogeneity over time was about twice as large in plasma as in CSF. It is about trial design and biomarker measurement, not treating, curing or preventing the disease.
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Understanding how the contents of consciousness, particularly perceptual awareness, change with the progression of AD is crucial for meaningful person-centred care.
Why it matters
This study found that brain responses linked to perceptual awareness are reduced in people with mild-to-moderate Alzheimer's and largely limited in severe Alzheimer's. It does not test any treatment or prevention, so it offers no direct implications for those goals.
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Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression.
Why it matters
This study identified genes associated with periodic and aperiodic EEG features in mild cognitive impairment, though no associations survived correction for multiple testing, and clustering based on these variants delineated subgroups differing in p-tau217 and verbal recall. These are preliminary genetic-EEG findings, not a treatment or cure.
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Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains.
Why it matters
This study developed a Spanish grammaticality judgment task and found that Alzheimer's disease and all three primary progressive aphasia variants had impaired comprehension of inflectional and transitivity information, while word order sensitivity was relatively preserved. It concerns language assessment, not treatment, cure or prevention.
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16/100
BackgroundEpidemiological studies increasingly associate several adult vaccinations with lower risk of Alzheimers disease (AD) and dementia, but the biological mechanisms underlying these observations remain unclear.
Why it matters
In this exploratory study, influenza, herpes zoster, pneumococcal and Td/Tdap vaccination were not associated with significant differences in the main plasma amyloid and tau panel, while hepatitis B vaccination was associated with lower tau markers though possibly due to confounding. These are preliminary observational biomarker findings, not evidence that vaccination prevents Alzheimer's disease.
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Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear.
Why it matters
This fine-mapping study found distinct HLA-II haplotypes associated with Alzheimer's disease risk and healthy longevity, with one protective haplotype linked to tau pathology and others to microglial HLA-II activation. These genetic and immune findings may inform understanding of disease mechanisms, not treatment or cure.
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Neuropsychiatric symptoms (NPS) are increasingly recognized as critical components of the disease progression in Alzheimers disease (AD), yet their relationship with neurodegeneration remain poorly characterized.
Why it matters
This deep learning study found that structural MRI-based neurodegeneration patterns predicted neuropsychiatric symptom scores and revealed distributed signatures differing most between cognitively normal and Alzheimer's participants. It is a modelling approach to understanding symptoms, not a treatment or cure.
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IntroductionNeuropsychiatric symptoms (NPS)--including aggression, psychosis, anxiety, apathy, and depression--affect up to 85% of individuals with Alzheimers disease (AD) and are among its most disabling and costly manifestations, accelerating cognitive and functional decline, institutionalization, mortality, and healthcare costs.
Why it matters
This study found that genetic ancestry assignment differed markedly from self-reported race and that neuropsychiatric symptom prevalence differed across ancestry groups. It concerns how race and ancestry are measured in research, not treatment, cure or prevention.
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Rapamycin, an FDA-approved inhibitor of the mammalian target of rapamycin (mTOR) pathway, has demonstrated promising anti-aging and neuroprotective effects.
Why it matters
This modelling study applied machine learning to rapamycin treatment data and identified biomarkers associated with treatment response, particularly in blood-based and inflammatory measures. It is a computational framework for small-sample studies and does not itself show that rapamycin treats or prevents Alzheimer's disease.
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BackgroundUp to 30% of individuals harboring core Alzheimers disease (AD) neuropathology--amyloid-{beta} (A{beta};A) and tau (T)--remain cognitively unimpaired.
Why it matters
In this cohort, cognitively unimpaired people with core Alzheimer's pathology had significantly higher cerebral blood flow than cognitively impaired people with the same pathology in regions vulnerable in early disease. This observational imaging finding may help explain why some people with pathology stay cognitively intact, but it is not a treatment or cure.
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AbstractO_ST_ABSBackgroundC_ST_ABSGlucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used for type 2 diabetes.
Why it matters
In this target trial emulation, starting a GLP-1 receptor agonist was associated with a small but statistically significant increase in dementia-free survival compared with sulfonylureas, while the average effect in the SGLT2 inhibitor comparison was not statistically significant. These are observational associations from electronic health records, not proof that the drug prevents Alzheimer's disease.
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16/100
Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes.
Why it matters
Alzheimer's disease genetic risk was enriched in peripheral immune, barrier and metabolic tissues, beyond what brain or microglial programs explain. This extends genetic models of the disease and does not test any treatment or prevention.
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Using the ADNI dataset, we found that the model realigned patients according to their clinical diagnoses.
Why it matters
This modelling work used the ADNI dataset and found that the model realigned patients according to their clinical diagnoses. It is a methodological tool for tracking disease progression and does not itself test any treatment, cure or prevention.
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BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging.
Why it matters
In this longitudinal cohort, a higher brain age gap was linked to poorer baseline cognition and predicted cognitive decline, with the strongest effects in people positive for both amyloid and tau. This is observational, so it shows an association that may help identify who is at risk, not a treatment or cure.
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INTRODUCTIONNovel capillary-blood collection methods have not yet been evaluated for a wide range of central nervous system (CNS) and neurodegenerative disease-related proteins.
Why it matters
A minimally invasive upper-arm capillary blood device measured some brain-related proteins, such as NfL and GFAP, in strong agreement with standard venous blood, but p-tau217 correlated poorly. The authors caution that biomarker-specific differences must be considered before this approach is used for other Alzheimer's biomarkers.
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Alzheimers disease (AD) unfolds over decades preceding cognitive symptoms, and measuring the full scope of its molecular complexity remains difficult.
Why it matters
By linking routine Alzheimer's blood biomarkers to thousands of plasma proteins, the researchers built progression-related modules that held up across 12 independent cohorts and were tied to cognitive decline. One synaptic module marked apparent neuronal resilience up to five years before estimated symptom onset.
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BACKGROUNDQuantitative amyloid-beta (A{beta})-PET is increasingly used in AD prevention trials.
Why it matters
Different amyloid-PET processing pipelines produced different positivity thresholds and disagreed most between 11 and 35 Centiloids, often in people who were accumulating amyloid. The authors stress that cut-point uncertainty and method choices matter when interpreting early-stage amyloidosis.
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus.
Why it matters
Long-read sequencing showed that many Alzheimer's disease GWAS loci contain structural variants and regulatory complexity that a single lead SNP does not capture. This refines understanding of genetic risk architecture and does not test any treatment or cure.
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16/100
Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood.
Why it matters
This genomic analysis linked obesity and type 2 diabetes to Alzheimer's disease through shared genes, mostly in peripheral immune and metabolic tissues, and nominated drug candidates for preclinical testing. The findings are computational and have not been tested as treatments in people.
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BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses.
Why it matters
Several plasma inflammatory markers were inversely associated with the CSF pTau181/Aβ42 ratio in pooled models, but formal biomarker-by-sex interactions did not survive correction. This is a cross-sectional biomarker study and does not test any treatment or prevention.
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Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable.
Why it matters
This study presents a computer model that predicts 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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Blood-based biomarkers could transform Alzheimer disease (AD) detection by enabling scalable, less invasive assessment of underlying pathology, yet their applicability across globally diverse populations remains uncertain.
Why it matters
This meta-analysis of 168 publications found that p-tau217, p-tau181 and glial fibrillary acidic protein showed the largest and most consistent differences across ethnoracial groups and healthcare settings. It supports blood biomarkers as a scalable, less invasive way to detect Alzheimer pathology, but says nothing about treating, curing or preventing it.
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.
- Personal mastery is associated with reduced sympathetic arousal in stressed Alzheimer caregivers
- Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease
- The effect of increased genetic risk for Alzheimer's disease on hippocampal and amygdala volume
- Decreased Serum Brain-Derived Neurotrophic Factor (BDNF) Levels in Patients with Alzheimer's Disease (AD): A Systematic Review and Meta-Analysis
- Integrated genomic meta-analysis identifies cell-type-specific signatures and targets in early Alzheimer's disease
- Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
- Progress in Machine Learning-Assisted Biosensors for Alzheimer’s Disease
- 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