ReviewThe Indian journal of medical research2018
New genetic players in late-onset Alzheimer's disease: Findings of genome-wide association studies.
Review in The Indian journal of medical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed.
- A Niacin-α-Lipoic Acid Hybrid Ameliorates Alzheimer's Disease Pathology in Mouse Models.ACS pharmacology & translational science · 2026Article
- The Role of circRNAs in the Pathological Mechanisms of Alzheimer's Disease: Potential Biomarkers for Diagnosis.Current neuropharmacology · 2025Review
- Role of Calcitriol and Vitamin D Receptor (International journal of molecular sciences · 2024Review
- Navigating the Frontiers of Machine Learning in Neurodegenerative Disease Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Brain structure and allelic associations in Alzheimer's disease.CNS neuroscience & therapeutics · 2023Article
- β-amyloid binds to microglia Dectin-1 to induce inflammatory response in the pathogenesis of Alzheimer's disease.International journal of biological sciences · 2023Article
- Is Drp1 a link between mitochondrial dysfunction and inflammation in Alzheimer's disease?Frontiers in molecular neuroscience · 2023Review
- Astrocytic and microglial cells as the modulators of neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2022Review
- Stearoyl-CoA Desaturase inhibition reverses immune, synaptic and cognitive impairments in an Alzheimer's disease mouse model.Nature communications · 2022Article
- Disease-specific interactome alterations via epichaperomics: the case for Alzheimer's disease.The FEBS journal · 2022Review
- Remembering your A, B, C's: Alzheimer's disease and ABCA1.Acta pharmaceutica Sinica. B · 2022Review
- Neuroinflammation as a Potential Therapeutic Target in Alzheimer's Disease.Clinical interventions in aging · 2022Review
- Alternative Splicing Regulation of Low-Frequency Genetic Variants in Exon 2 ofInternational journal of molecular sciences · 2021Article
- Neuroinflammation in Alzheimer's Disease.Biomedicines · 2021Review
- Gauging the role and impact of drug interactions and repurposing in neurodegenerative disorders.Current research in pharmacology and drug discovery · 2021Review
- The Other Side of Alzheimer's Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers.Journal of personalized medicine · 2020Review
- Parkinson disease and the immune system - associations, mechanisms and therapeutics.Nature reviews. Neurology · 2020Review
- Therapeutic Lessons to be Learned From the Role of Complement Regulators as Double-Edged Sword in Health and Disease.Frontiers in immunology · 2020Review
- Data-Driven Modeling of Knowledge Assemblies in Understanding Comorbidity Between Type 2 Diabetes Mellitus and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2020Article
- The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Late-onset Alzheimer's disease (LOAD) or sporadic AD is the most common form of AD. The precise pathogenetic changes that trigger the development of AD remain largely unknown. Large-scale genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms in multiple genes which are associated with AD; most notably, these are ABCA7, bridging integrator 1 (B1N1), triggering receptor expressed on myeloid cells 2 (TREM2), CD33, clusterin (CLU), complement receptor 1 (CRI), ephrin type-A receptor 1 (EPHA1), membrane-spanning 4-domains, subfamily A (MS4A) and phosphatidylinositol binding clathrin assembly protein (PICALM) genes. The proteins coded by the candidate genes participate in a variety of cellular processes such as oxidative balance, protein metabolism, cholesterol metabolism and synaptic function. This review summarizes the major gene loci affecting LOAD identified by large GWASs. Tentative mechanisms have also been elaborated in various studies by which the proteins coded by these genes may exert a role in AD pathogenesis have also been elaborated. The review suggests that these may together affect LOAD pathogenesis in a complementary fashion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.