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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Potential pharmacogenetic biomarkers for AD have been identified; however, it is still necessary to conduct further research into other populations and to identify new biomarkers.
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48/100
Patients with Alzheimer's disease (AD) and Parkinson's disease (PD) often have overlap in clinical presentation and brain neuropathology suggesting that these two diseases share common underlying mechanisms.
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Functional phenotypes (e.g., subcortical surface representation), which commonly arise in imaging genetic studies, have been used to detect putative genes for complexly inherited neuropsychiatric and neurodegenerative disorders.
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This transcriptomic network analysis of 19 brain regions provides a comprehensive assessment of the critical molecular pathways associated with AD pathology and offers new insights into molecular mechanisms underlying selective regional vulnerability to AD at different stages of the progression of cognitive compromise and development of the canonical neuropathological lesions of AD.
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There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration.
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48/100
The mean age was 51 ± 12 years. Forty-two of the patients had OSAS.
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Mutations in the CHCHD10 gene have been recently identified in a large family with a complex phenotype variably associating frontotemporal dementia (FTD) with amyotrophic lateral sclerosis (ALS), cerebellar ataxia, myopathy, and hearing impairment.
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Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD).
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Age-related cognitive decline is likely promoted by accumulated brain injury due to chronic conditions of aging, including neurodegenerative and vascular disease.
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ApoE-4 was strongly associated with AD in this sample (allele frequency = 0.46 vs. 0.14 in controls, p < 0.000001).
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An association between the 19q13.2 chromosomal region and Alzheimer's disease (AD) has been reported in AD families and for sporadic AD.
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Apolipoprotein E (apoE) is associated with Alzheimer's neurofibrillary tangles and beta-amyloid protein in senile plaques.
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Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD).
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47/100
Recent work has identified dozens of non-coding loci for Alzheimer's disease (AD) risk, but their mechanisms and AD transcriptional regulatory circuitry are poorly understood.
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The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood.
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Polygenic Risk Scores (PRS) for AD offer unique possibilities for reliable identification of individuals at high and low risk of AD.
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Single-cell RNA-sequencing (scRNA-Seq) is widely used to reveal the heterogeneity and dynamics of tissues, organisms, and complex diseases, but its analyses still suffer from multiple grand challenges, including the sequencing sparsity and complex differential patterns in gene expression.
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Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis.
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Clinical trials of novel therapeutics for Alzheimer's Disease (AD) have consumed a large amount of time and resources with largely negative results.
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Large studies (e.g. UK Biobank) are increasingly used for GWAS and Mendelian randomization (MR) studies.
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Genome-wide association studies (GWAS) have identified many risk loci for Alzheimer's disease (AD) 1,2 , but how these loci confer AD risk is unclear.
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Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 .
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Higher HOMA-IR was associated with higher sAβPPβ and Aβ42 .
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We confirm that variation in/near APOE/TOMM40 (P = 6 × 10(-14)) alters PCA risk, but with smaller effect than for typical AD (PCA: odds ratio [OR] = 2.03, typical AD: OR = 2.83, P = .0007).
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There is no consensus for a blood-based test for the early diagnosis of Alzheimer's disease (AD).
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.
- Spatial Transcriptomic Analysis Identifies a SERPINA3-Expressing Astrocytic State Associated with the Human Neuritic Plaque Microenvironment
- Genetics of Alzheimer's Disease in the African American Population
- Genetics of Alzheimer's Disease: the Importance of Polygenic and Epistatic Components
- Rare coding variants in the phospholipase D3 gene confer risk for Alzheimer's disease
- Genome-Wide Association Study of Incident Dementia in a Community-Based Sample of Older Subjects
- [Genetic Background for Alzheimer's Disease: Knowledge Accumulated from AD GWAS]
- Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era
- Whole-Genome Sequencing of a Healthy Aging Cohort
- Shared Genetic Etiology between Alzheimer's Disease and Blood Levels of Specific Cytokines and Growth Factors
- Plasma biomarkers and genetics in the diagnosis and prediction of Alzheimer's disease