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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Baseline sleep disturbance was associated with a faster rate of longitudinal CSF Aβ42 decline.
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Lewy body dementia (LBD) is the second most prevalent dementia, however most genetic risk remains uncharacterized.
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The use of quantitative endophenotypes in genetic studies may provide greater power, allowing for the use of powerful statistical methods and a biological model for the effects of the disease-associated genetic variation.
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Genome-wide association studies have discovered numerous genomic loci associated with Alzheimer's disease (AD); yet the causal genes and variants are incompletely identified.
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74/100
The APOE ε4 allele remains the strongest genetic risk factor for sporadic Alzheimer's disease and the APOE ε2 allele the strongest genetic protective factor after multiple large scale genome-wide association studies and genome-wide association meta-analyses.
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The disclosure of APOE genotyping results to adult children of patients with Alzheimer's disease did not result in significant short-term psychological risks.
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Three AD subtypes were identified. Subtype 1, enriched in RNA metabolism pathways, showed the mildest atrophy and slowest cognitive decline.
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73/100
Cognitive impairment was observed in 65 patients (42.5%) during a mean follow-up of 37.7 ± 12.4 months.
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Previously reported pathogenic variants in the six genes were identified in 1.35% of EOAD (3/223) and 6.58% of EOnonAD (5/76).
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Genome-wide association studies (GWAS) of Alzheimer's disease are predominantly carried out in European ancestry individuals despite the known variation in genetic architecture and disease prevalence across global populations.
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The primary genetic risk factor for late onset Alzheimer's disease (LOAD) is the APOE4 allele of Apolipoprotein E (APOE) gene.
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Age-related hearing loss is linked to loneliness and poorer cognitive health, but it remains unclear whether loneliness helps explain associations between hearing difficulties and cognitive performance or dementia, and whether these patterns reflect causal pathways or shared underlying liability.
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Genetic discoveries of Alzheimer's disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials.
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Genome-wide association studies have mainly relied on common HapMap sequence variations.
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Recently, several genome-wide association studies (GWASs) have led to the discovery of nine new loci of genetic susceptibility in Alzheimer's disease (AD).
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The Core 1 biomarker PGSs predicted AD pathology and associated cognitive performance better than the AD PGSs in both populations.
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To date, DNA methylation is the best characterized epigenetic modification in Alzheimer's disease.
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To define Alzheimer's disease with biomarkers rather than clinical assessment, we assessed prediction of research-diagnosed disease status using these biomarkers and tested genetic variants associated with the biomarkers that may reflect more accurately the risk of biochemically defined Alzheimer's disease instead of the risk of dementia.
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SORL1 is associated with AD in the Hong Kong Chinese population.
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Approximately 30% of older adults exhibit the neuropathological features of Alzheimer's disease without signs of cognitive impairment.
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More than 20 genetic loci have been associated with risk for Alzheimer's disease (AD), but reported genome-wide significant loci do not account for all the estimated heritability and provide little information about underlying biological mechanisms.
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First, we mapped SVs across 81 AD risk loci and discovered 22 SVs in linkage disequilibrium (LD) with GWAS lead variants and directly associated with the phenotypes tested.
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Targeted analysis of 20 SNPs that were reported to be associated with ADRD revealed that six were significantly associated with dual-disease outcomes, specifically congestive heart failure and cancer.
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70/100
A one standard deviation increase in AD-PGS was associated with an accelerated time to dementia diagnosis by 4.8 months.
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Both intervention and control groups showed cognitive improvement over 24 weeks, with greater gains in the intervention arm.
From across this topic
10 of the 933 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.
- Mitochondrial DNA copy number in neurodegenerative diseases: a global meta-analysis of 156 comparisons across 76 studies
- Genome-Wide Association Studies, Field Synopses, and the Development of the Knowledge Base on Genetic Variation and Human Diseases
- Mendelian randomization study on the causal effect of chickenpox on dementia
- Integrative multi-omics approaches identify molecular pathways and improve Alzheimer's disease risk prediction
- microRNA-33 Regulates ApoE Lipidation and Amyloid-β Metabolism in the Brain
- Genome-wide association study of abnormal elevation of ALT in patients exposed to atabecestat
- Shared Causal Paths underlying Alzheimer's dementia and Type 2 Diabetes
- Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) Trial: Genetic Resource for Precision Nutrition
- Single Cell Sequencing Technology and Its Application in Alzheimer's Disease
- Crosslinking of apolipoprotein E by products of lipid peroxidation