ReviewCellular and molecular life sciences : CMLS2018
Impact of late-onset Alzheimer's genetic risk factors on beta-amyloid endocytic production.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Functional relationships linking C99/APP-βCTF dimerization, proteostasis disruption, and organelle dysfunction.Cell communication and signaling : CCS · 2026Article
- The impact of high-sugar diets on central nervous system disorders: mechanisms, pathogenesis, and dietary implication.Annals of medicine · 2025Review
- APP lysine 612 lactylation ameliorates amyloid pathology and memory decline in Alzheimer's disease.The Journal of clinical investigation · 2025Article
- Dynamic functional network connectivity and its association with lipid metabolism in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- Increasing the Survival of a Neuronal Model of Alzheimer's Disease Using Docosahexaenoic Acid, Restoring Endolysosomal Functioning by Modifying the Interactions between the Membrane Proteins C99 and Rab5.International journal of molecular sciences · 2024Article
- Clathrin mediated endocytosis in Alzheimer's disease: cell type specific involvement in amyloid beta pathology.Frontiers in aging neuroscience · 2024Review
- Apolipoprotein E intersects with amyloid-β within neurons.Life science alliance · 2023Article
- The Cleavage-Specific Tau 12A12mAb Exerts an Anti-Amyloidogenic Action by Modulating the Endocytic and Bioenergetic Pathways in Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2023Article
- Upregulation of endocytic protein expression in the Alzheimer's disease male human brain.Aging brain · 2023Article
- AP2S1 regulates APP degradation through late endosome-lysosome fusion in cells and APP/PS1 mice.Traffic (Copenhagen, Denmark) · 2023Article
- Crosstalk between the Rho and Rab family of small GTPases in neurodegenerative disorders.Frontiers in cellular neuroscience · 2023Review
- Amphiphysin AoRvs167-Mediated Membrane Curvature Facilitates Trap Formation, Endocytosis, and Stress Resistance inPathogens (Basel, Switzerland) · 2022Article
- Mitochondrial Dysregulation and the Influence in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2022Article
- The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- Mitochondrial Disruption by Amyloid Beta 42 Identified by Proteomics and Pathway Mapping.Cells · 2021Article
- A Super-Resolved View of the Alzheimer's Disease-Related Amyloidogenic Pathway in Hippocampal Neurons.Journal of Alzheimer's disease : JAD · 2021Article
- Transmissible Endosomal Intoxication: A Balance between Exosomes and Lysosomes at the Basis of Intercellular Amyloid Propagation.Biomedicines · 2020Review
- High glucose-mediated PICALM and mTORC1 modulate processing of amyloid precursor protein via endosomal abnormalities.British journal of pharmacology · 2020Article
- Upregulation of RIN3 induces endosomal dysfunction in Alzheimer's disease.Translational neurodegeneration · 2020Article
- Intracellular Trafficking Mechanisms of Synaptic Dysfunction in Alzheimer's Disease.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The increased production of the 42 aminoacids long beta-amyloid (Aβ42) peptide has been established as a causal mechanism of the familial early onset Alzheimer's disease (AD). In contrast, the causal mechanisms of the late-onset AD (LOAD), that affects most AD patients, remain to be established. Indeed, Aβ42 accumulation has been detected more than 30 years before diagnosis. Thus, the mechanisms that control Aβ accumulation in LOAD likely go awry long before pathogenesis becomes detectable. Early on, APOE4 was identified as the biggest genetic risk factor for LOAD. However, since APOE4 is not present in all LOAD patients, genome-wide association studies of thousands of LOAD patients were undertaken to identify other genetic variants that could explain the development of LOAD. PICALM, BIN1, CD2AP, SORL1, and PLD3 are now with APOE4 among the identified genes at highest risk in LOAD that have been implicated in Aβ42 production. Recent evidence indicates that the regulation of the endocytic trafficking of the amyloid precursor protein (APP) and/or its secretases to and from sorting endosomes is determinant for Aβ42 production. Thus, here, we will review the described mechanisms, whereby these genetic risk factors can contribute to the enhanced endocytic production of Aβ42. Dissecting causal LOAD mechanisms of Aβ42 accumulation, underlying the contribution of each genetic risk factor, will be required to identify therapeutic targets for novel personalized preventive strategies.
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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.