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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First recognized as a major determinant in lipoprotein metabolism and cardiovascular disease, apolipoprotein (apo) E has emerged as an important molecule in several biological processes not directly related to its lipid transport function, including Alzheimer's disease and cognitive function, immunoregulation, and possibly even infectious diseases.
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Apolipoprotein E (APOE = gene, apoE = protein) plays a central role in plasma lipoprotein metabolism and in lipid transport within tissues.
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Mutations in the human presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease.
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Alzheimer's disease (AD) is unique in medicine in that millions of people suffer from what appears to be the same form of disease, and unlike most other late-onset diseases, the genetic etiologies have been well identified.
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Aberrant expression of the amyloid precursor protein (APP) gene may contribute to the beta-amyloid deposition seen in Alzheimer's disease and Down syndrome patients.
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Recent evidence indicates that apolipoprotein E (ApoE) plays a central role in the hippocampal response to injury.
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This work suggests that although parity history and PSEN2 deficiency exert individual differing age-related effects on cognition and neurobiology, they do not act synergistically.
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Active PTB was associated with widespread transcriptional remodeling, with 1,389 dysregulated genes organized into 16 PTB-associated co-expression modules.
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Multi-subject spatial transcriptomics is increasingly used to identify molecular differences across individuals and conditions while resolving where in tissue those differences occur.
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Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation.
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Blood-based biomarkers for Alzheimer disease and related dementias have been validated largely in populations of European ancestry.
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The full cohort included 1044 participants, of whom 779 comprised the proteomics cohort.
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Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology.
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Psychosis is a neuropsychiatric feature found across neurodegenerative conditions including Alzheimer’s disease (AD) and Parkinson’s disease (PD).
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Alzheimer’s disease (AD) develops over decades, but biological processes underlying susceptibility during midlife remain poorly understood.
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Polygenic risk scores (PRSs) have improved substantially in predictive performance, yet results remain difficult to compare across studies that differ in cohorts, phenotype definitions, and evaluation procedures.
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Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease.
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DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD).
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For a long time, the protein coding potential of our genome was underestimated.
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Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant.
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In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation.
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Parental history of dementia is a risk factor for Alzheimer’s disease, although the mechanisms underlying this association remain poorly understood.
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The blood-based biomarker (BBM) profiles associated with genetic susceptibility to Alzheimer’s disease (AD) in general older populations remain poorly understood.
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While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses.
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This study represents the largest PD AAO meta-analysis in European-ancestry populations to date.
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.
- Integrative network analysis of nineteen brain regions identifies molecular signatures and networks underlying selective regional vulnerability to Alzheimer's disease
- Increased Plasma S-Adenosylhomocysteine–Accelerated Atherosclerosis Is Associated With Epigenetic Regulation of Endoplasmic Reticulum Stress in apoE −/− Mice
- The involvement of lipids in Alzheimer's disease
- A genomic pathway approach to a complex disease: axon guidance and Parkinson disease
- Education, intelligence, and amyotrophic lateral sclerosis: A Mendelian randomization study
- Machine learning identifies candidates for drug repurposing in Alzheimer's disease
- Apolipoprotein E and lipid homeostasis in the etiology and treatment of sporadic Alzheimer's disease
- A novel biochemical analysis for ApoE4 quantification in plasma and discrimination of homozygous and heterozygous APOE ε4 carriers
- Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer's disease, Parkinson's disease, and related disorders
- Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries