ArticleFuture neurology2012
The role of intracellular trafficking and the VPS10d receptors in Alzheimer's disease.
Article in Future neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Dissecting the genetic overlap between severe mental disorders and markers of cellular aging: Identification of pleiotropic genes and druggable targets.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- SorCS3 promotes the internalization of p75Cell death & disease · 2022Article
- Insights into the mechanisms of non-coding RNAs' implication in the pathogenesis of Alzheimer's disease.EXCLI journal · 2022Review
- Insights into lncRNAs in Alzheimer's disease mechanisms.RNA biology · 2021Review
- Urinary metabolic phenotyping for Alzheimer's disease.Scientific reports · 2020Article
- Integrated analysis and network pharmacology approaches to explore key genes of Xingnaojing for treatment of Alzheimer's disease.Brain and behavior · 2020Article
- Peripheral Blood MicroRNA Expression Profiles in Alzheimer's Disease: Screening, Validation, Association with Clinical Phenotype and Implications for Molecular Mechanism.Molecular neurobiology · 2016Article
- Pericytes of the neurovascular unit: key functions and signaling pathways.Nature neuroscience · 2016Review
- Elucidating molecular phenotypes caused by the SORL1 Alzheimer's disease genetic risk factor using human induced pluripotent stem cells.Cell stem cell · 2015Article
- Parkinson's disease genes VPS35 and EIF4G1 interact genetically and converge on α-synuclein.Neuron · 2015Article
- α(2A) adrenergic receptor promotes amyloidogenesis through disrupting APP-SorLA interaction.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
In Alzheimer's disease, the key pathological culprit is the amyloid-β protein, which is generated through β- and γ-secretase cleavage of the amyloid-β precursor protein (APP). Both the secretases and amyloid-β precursor protein are transmembrane proteins that are sorted via the trans-Golgi network and the endosome through multiple membranous compartments of the cell. The coat complex clathrin controls the sorting from the cell surface and the trans-Golgi network to the endosome. Instead, the retromer controls the reverse transport from the endosome to the trans-Golgi network. The retromer contains two subprotein complexes: the cargo-selective subcomplex consisting of VPS35, VPS29 and VPS26 and the membrane deformation subcomplex consisting of Vps5p, Vps17p, SNX 1/2 and possibly SNX 5/6 or SNX 32 in mammals. Cargo molecules of the retromer include the VPS10 receptor proteins SORL1, SORT1, SORCS1, SORCS2 and SORCS3. There is increasing evidence through cell biology and animal and genetic studies that components of the retromer and the VPS10d receptor family play a role in the etiology of Alzheimer's disease. This article reviews and summarizes this current evidence.
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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.