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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The two sites associated with interactions between AD and a metabolic condition could explain the influence that those conditions have on the risk for AD and are prime candidates for future study.
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Educational attainment and physical activity PRSs were associated with AD in both sexes.
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Many biological quantities in omics are inherently periodic or directional, including circadian phase, cell-cycle position, and cellular orientation.
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Genetically predicted BP raises WMH in European and Japanese ancestry.
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Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood.
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Cerebrospinal fluid (CSF) contains brain derived proteins that can be leveraged as biomarkers for Alzheimer’s disease (AD) and other neurodegenerative diseases.
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We then integrated healthy retinal expression, AD retinal proteomics, and PD aqueous-humor proteomics with the brain-concordance results.
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16/100
Severe cognitive decline due to dementia is an important clinical indicator signaling neurodegeneration.
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Alzheimer’s disease is a progressive, currently irreversible, neurodegenerative disorder associated with the accumulation of β-Amyloid (Aβ) plaques between cells and tau (τ) tangles within cells.
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Apolipoprotein E (APOE) genotype is theorised to influence dementia risk partly through effects on blood–brain barrier (BBB) function, but clinical studies examining APOE effects on BBB biomarkers report inconsistent results.
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Identifying early life biomarkers of suboptimal aging trajectories could help design interventions to delay or even prevent the onset of pathological conditions in older adulthood.
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In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks.
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Vascular dementia (VaD) is a leading cause of cognitive decline with no disease-modifying therapies.
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We identified 27 phenotypes associated with APOE, mainly in neurological and lipid-related traits.
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Genetic studies have identified thousands of variants associated with brain-related traits.
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MicroRNAs (miRNAs) are implicated in Alzheimer's disease (AD), but research has focused on individual miRNAs and direct targets.
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Formalin-fixed, paraffin-embedded (FFPE) brain tissue is a major archival resource, yet its suitability for high-density DNA methylation profiling is limited by fixation-induced DNA fragmentation and crosslinking.
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Inverse-variance weighted MR indicated that genetically predicted focal epilepsy with hippocampal sclerosis was associated with increased odds of AD (OR=3.99, 95% CI 1.17–13.61; P=0.027).
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Immunofluorescence staining of FFPE tissue following Xenium processing also preserves cellular morphology, allowing the morphological complexity of distinct cell types to be captured and quantitated, especially for glial cells with highly ramified processes.
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16/100
Parkinson disease (PD) was examined in four primary adult-brain GEO cohorts (GSE49036, GSE20141, GSE8397, GSE7621) using a frozen 468-gene redox, metal, xenobiotic, and barrier panel.
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Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons.
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Familial Alzheimer’s disease (fAD) is an early-onset form of AD caused by autosomal-dominant variants in APP, PSEN1, or PSEN2, with PSEN1 accounting for most genetically defined cases [1].
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TAR DNA-binding protein 43 (TDP-43) is a key pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and a critical regulator of RNA splicing.
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Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases.
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In brain, inverse-variance random-effects meta-analysis (DerSimonian–Laird) across six independent postmortem adult-brain GEO cohorts (GSE33000, GSE132903, GSE173955, GSE159699, GSE5281, GSE48350) yielded 458 analyzable panel genes, 167 at Benjamini–Hochberg FDR < 0.05, and 141 high-confidence genes (FDR < 0.05, measured in at least three cohorts, direction-concordant in at least 70% of cohorts, and nominally significant in at least two cohorts).
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.
- Shared genetic risk loci between Alzheimer's disease and related dementias, Parkinson's disease, and amyotrophic lateral sclerosis
- A single-cell and spatial RNA-seq database for Alzheimer's disease (ssREAD)
- Genetic architectures of psychiatric disorders: the emerging picture and its implications
- Drug repositioning based on the heterogeneous information fusion graph convolutional network
- Improving genetic risk modeling of dementia from real-world data in underrepresented populations
- APOE Variants in an Iberian Alzheimer Cohort Detected through an Optimized Sanger Sequencing Protocol
- Integrated Proteomic and Phosphoproteomic Profiling Reveals Distinct Disease- and Age-Related Molecular Alterations in the Retina and Hippocampus of APP/PS1/MAPT Mice
- Unlocking Sensitive Data with SPHERE in the Age of AI
- [Early-onset familial Alzheimer's disease with spastic paraparesis associated with PSEN1 gene]
- DNA methylation in the human cerebral cortex is dynamically regulated throughout the life span and involves differentiated neurons