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 APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear.
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Cerebral small vessel disease (cSVD) is a leading cause of ischaemic and haemorrhagic stroke and a major contributor to dementia.
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ADVP V1.0 (February 2021) catalogs 6,990 associations related to disease-risk, expression quantitative traits, endophenotypes, or neuropathology.
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The success of genome-wide association studies (GWAS) completed in the last 15 years has reinforced a key fact: polygenic architecture makes a substantial contribution to variation of susceptibility to complex disease, including Alzheimer's disease.
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It enables robust identification of signaling pathways enriched in disease susceptibility loci.
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In recent decades, our understanding of the molecular changes involved in neurodegenerative diseases has been transformed.
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In silico reuse of old drugs (also known as drug repositioning) to treat common and rare diseases is increasingly becoming an attractive proposition because it involves the use of de-risked drugs, with potentially lower overall development costs and shorter development timelines.
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In this study, a drug repositioning algorithm based on a deep autoencoder and adaptive fusion was proposed to mitigate the problems of decreased precision and low-efficiency multisource data fusion caused by data sparseness.
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The genetic locus containing the WWOX and MAF genes was implicated as a clinical Alzheimer's disease (AD) risk locus in two recent large meta-analytic genome wide association studies (GWAS).
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An arginine-rich apolipoprotein was discovered 50 years ago and became known as apolipoprotein E (ApoE) 10 years later.
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Though apolipoprotein E ε4 (APOE ε4) is a major genetic risk factor for late-onset Alzheimer's disease, its association with depression remains controversial.
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Age-related macular degeneration (AMD) is a multifactorial retinal disorder that is a major global cause of severe visual impairment.
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The treatment of complex and multifactorial diseases constitutes a big challenge in day-to-day clinical practice.
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Late-onset Alzheimer's disease (AD) has a significant genetic and immunological component, but the molecular mechanisms through which genetic and immunity-related risk factors and their interplay contribute to AD pathogenesis are unclear.
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Since the identification of the apolipoprotein E (apoE) *ε4 allele as a major genetic risk factor for late-onset Alzheimer's disease, significant efforts have been aimed at elucidating how apoE4 expression confers greater brain amyloid-β (Aβ) burden, earlier disease onset and worse clinical outcomes compared to apoE2 and apoE3.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with a complex genetic etiology.
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Alzheimer's disease (AD) can be either sporadic or familial, and familial forms of AD accounts for only 5% of the cases.
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Alzheimer's disease (AD) is the most common form of dementia, currently affecting 35 million people worldwide.
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42 common genes were identified between OSA and dementia which were primarily linked to the G-coupled protein receptor (GPCR) and olfactory pathways.
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The high prevalence of Alzheimer's disease (AD) among the elderly population and its lack of effective treatments make this disease a critical threat to human health.
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Late-onset Alzheimer's disease (LOAD), the most common cause of dementia, and a huge global health challenge, is a neurodegenerative disease of uncertain aetiology.
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Alzheimer's disease (AD) is the most common senile neurodegenerative disease characterized by progressive cognitive dysfunction, psychological and behavioral abnormalities, and impaired ability of activities of daily living.
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A multi-stage variable selection method is introduced for detecting association signals in structured brain-wide and genome-wide association studies (brain-GWAS).
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Novel therapeutic strategies for Alzheimer's disease (AD) are of the greatest priority given the consistent failure of recent clinical trials focused on Aβ or pTau.
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In this issue of Neuron, Wang et al. employ an impressive multi-omics approach, including gene co-expression network analyses and drug repositioning, to normalize disease-disrupted gene modules and identify a therapeutically relevant driver of Alzheimer's disease.
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.
- A History of Repeated Alcohol Intoxication Promotes Cognitive Impairment and Gene Expression Signatures of Disease Progression in the 3xTg Mouse Model of Alzheimer's Disease
- Genome-wide association study of Alzheimer's disease CSF biomarkers in the EMIF-AD Multimodal Biomarker Discovery dataset
- Liver-Specific Polygenic Risk Score Is Associated with Alzheimer's Disease Diagnosis
- Screening of CHCHD10 in a French cohort confirms the involvement of this gene in frontotemporal dementia with amyotrophic lateral sclerosis patients
- RNA Isoform Diversity in Human Neurodegenerative Diseases
- Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses
- Phenotype Scoring of Population Scale Single-Cell Data Dissects Alzheimer's Disease Complexity
- Alzheimer's disease genetic risk score and neuroimaging in the FINGER lifestyle trial
- A genome-wide association meta-analysis of all-cause and vascular dementia
- CausalDiffChem: Causal Network Restoration for Therapeutic Prioritization and Repurposing Across Diseases