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.
-
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints.
-
How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear.
-
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects.
-
Transcriptomic and proteomic studies have consistently demonstrated substantial molecular heterogeneity across patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, leading to the proposal of multiple disease subtypes.
-
16/100
Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia.
-
ORIGIN-PD enables rational enrichment for NLRP3/NF-κB inhibitor trials by identifying patients with inflammatory involvement.
-
Individuals with comparable Alzheimer’s disease (AD) pathology can differ markedly in cognition, but the molecular nature of this heterogeneity remains unclear.
-
Alzheimer’s disease (AD) target evidence is distributed across biological, chemical, structural, regulatory, and trial-registry sources, complicating reproducible target evaluation and modeling.
-
Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association.
-
Partitioned-heritability studies have shown which tissues carry the heritability of complex traits, but whether the regulatory layer whose annotations are most informative for heritability within a tissue differs between traits has not been tested, because measured annotations for different layers come from different sets of biosamples.
-
Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved.
-
Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations.
-
Conventional, cohort-based staging exhibited profound topographical inversion, yielding negative correlations for TDP-43 ( ρ = -0.9113, p < 0.001) and α-synuclein ( ρ = -0.8660, p = 0.003) sub-cohorts.
-
Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk.
-
Based on the exacerbated AD pathological features and transcriptomic alterations observed in Arf4 knockdown animals, ARF4 appears to play a critical role in AD resilience and may represent a potential prognostic factor worthy of further investigation.
-
Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies.
-
This study investigated volumetric MRI differences of the thalamic nuclei in asymptomatic young adult C9orf72 expansion carriers compared to non-carriers, and examined spatial associations with normative thalamic transcriptomics from 8 weeks post-conception through middle age.
-
The disorders fell into one of three categories based on the topographic relationship of the disease-specific and healthy networks.
-
In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape.
-
The reproducibility crisis in biomedical research calls for re-evaluation of how common analytic approaches affect results.
-
Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping.
-
Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity.
-
Sequence models predict the molecular effects of genetic variation, yet their contribution to interpreting Alzheimer’s disease (AD) association signals remains uncertain.
-
Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae.
-
These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise.
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.
- Human neocortical expansion involves glutamatergic neuron diversification
- Overcoming segmentation bottlenecks in brain tissue for spatial proteomic inference at population scale
- Risk of Alzheimer's disease and related dementia by sex and race/ethnicity: The Multiethnic Cohort Study
- Genetic influences on brain and cognitive health and their interactions with cardiovascular conditions and depression
- scMD facilitates cell type deconvolution using single-cell DNA methylation references
- APOEε4 potentiates the relationship between amyloid-β and tau pathologies
- Epigenetic dysregulation of enhancers in neurons is associated with Alzheimer’s disease pathology and cognitive symptoms
- Presenilin Gene Mutation-associated Psychosis: Phenotypic Characteristics and Clinical Implications
- Integrating human brain proteomes with genome-wide association data implicates new proteins in Alzheimer's disease pathogenesis
- Sex differences in the progression of glucose metabolism dysfunction in Alzheimer's disease