ReviewMolecular neurobiology2016
The Role of Retromer in Alzheimer's Disease.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Proteome-wide Mendelian randomization identifies causal plasma proteins in frontotemporal dementia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Pooled it
- Article
- The aldehyde dehydrogenase 2 rs671 variant enhances amyloid β pathology.Nature communications · 2024Article
- Endocytosis and Alzheimer's disease.GeroScience · 2024Review
- The emerging roles of retromer and sorting nexins in the life cycle of viruses.Virologica Sinica · 2022Review
- Retromer dysfunction at the nexus of tauopathies.Cell death and differentiation · 2021Review
- Endosomal Trafficking in Alzheimer's Disease, Parkinson's Disease, and Neuronal Ceroid Lipofuscinosis.Molecular and cellular biology · 2020Review
- Mitochondrial Dysfunction, Oxidative Stress, and Neuroinflammation: Intertwined Roads to Neurodegeneration.Antioxidants (Basel, Switzerland) · 2020Review
- Generation and Release of Mitochondrial-Derived Vesicles in Health, Aging and Disease.Journal of clinical medicine · 2020Review
- Vps35 Deficiency Impairs Cdk5/p35 Degradation and Promotes the Hyperphosphorylation of Tau Protein in Retinal Ganglion Cells.Investigative ophthalmology & visual science · 2020Article
- Extracellular Vesicles and Damage-Associated Molecular Patterns: A Pandora's Box in Health and Disease.Frontiers in immunology · 2020Review
- Review
- RAB10: an Alzheimer's disease resilience locus and potential drug target.Clinical interventions in aging · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retromer complex is an important component of the endosomal protein sorting machinery and mediates protein cargoes from endosomes to the trans-Golgi network (TGN) by retrograde pathway or to the cell surface through recycling pathway. Studies show that retromer and its receptors can make amyloid precursor protein (APP)/β-site APP-cleaving enzyme 1 (BACE1) away endosomes that reduces the production of amyloid β (Aβ). And, tetramer is also found to regulate phagocytic receptors to the plasma membrane of microglia, where some phagocytic receptors take part in Aβ clearance. Therefore, disruption of retromer will increase the production of Aβ. Recently, a plausible relationship between disturbance of retromer and tauopathies is raised. Retromer dysfunction may result in decreasing the clearance of extracellular tau and the level of cathepsin D, which enables tau-induced neurotoxicity. This review article summarizes the structure and function of retromer and its role in pathogenesis of AD. In the end, retromer may provide a potential therapeutic strategy for the treatment of AD.
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What OpenQuestion holds
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.