ArticleMolecular psychiatry2020
Full recovery of the Alzheimer's disease phenotype by gain of function of vacuolar protein sorting 35.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 32 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
32 citing papers in PubMed, 50 citations in OpenAlex.
- PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity.The Journal of cell biology · 2025Article
- Review
- CREB3L2-ATF4 heterodimerization defines a transcriptional hub of Alzheimer's disease gene expression linked to neuropathology.Science advances · 2023Article
- Receptor Recycling by Retromer.Molecular and cellular biology · 2023Review
- Review
- Critical Role of Neuronal Vps35 in Blood Vessel Branching and Maturation in Developing Mouse Brain.Biomedicines · 2022Article
- Retromer dysfunction in amyotrophic lateral sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CROP: a retromer-PROPPIN complex mediating membrane fission in the endo-lysosomal system.The EMBO journal · 2022Article
- Pharmacological modulation of autophagy for Alzheimer's disease therapy: Opportunities and obstacles.Acta pharmaceutica Sinica. B · 2022Review
- Association of Retromer Deficiency and Tau Pathology in Down Syndrome.Annals of neurology · 2022Article
- Mutations inNeural regeneration research · 2022Article
- Machine learning prediction and tau-based screening identifies potential Alzheimer's disease genes relevant to immunity.Communications biology · 2022Article
- The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease.Cell reports · 2022Article
- Review
- Dysfunction of the retromer complex system contributes to amyloid and tau pathology in a stem cell model of Down syndrome.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- Immunogenetic Determinants of Parkinson's Disease Etiology.Journal of Parkinson's disease · 2022Review
- Beware of Misdelivery: Multifaceted Role of Retromer Transport in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- Retromer regulates the lysosomal clearance of MAPT/tau.Autophagy · 2021Article
- Expression of Low Level of VPS35-mCherry Fusion Protein Diminishes Vps35 Depletion Induced Neuron Terminal Differentiation Deficits and Neurodegenerative Pathology, and Prevents Neonatal Death.International journal of molecular sciences · 2021Article
- Opposing functions for retromer and Rab11 in extracellular vesicle traffic at presynaptic terminals.The Journal of cell biology · 2021Article
Corrections and comments
- Retraction · 2022-10-18Duplication of/in Article ·
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Deficit in retromer complex function secondary to lower levels of one of its major components, the vacuolar protein sorting 35 (VPS35), has been reported in Alzheimer's disease (AD) brains. VPS35 genetic reduction results in increased Aβ levels and synaptic pathology in mouse models of the disease. However, whether restoration of its levels has an effect on the AD-like phenotype which includes Aβ plaques, tau tangles and memory impairments remain unknown. In this paper, we investigated the effect of VPS35 gene delivery into the central nervous system on the development of the neuropathology and behavioral deficits of the triple transgenic (3xTg) mice. Compared with controls, animals overexpressing VPS35 had an amelioration of spatial learning and working memory, which associated with a significant reduction in Aβ levels and deposition and tau phosphorylation. Additionally, the same animals had a significant improvement of synaptic pathology and neuroinflammation. In vitro study confirmed that VPS35 up-regulation by reducing total levels of APP and results in a significant decrease in its metabolic products. Our results demonstrate for the first time that VPS35 is directly involved in the development of AD-like phenotype, and for this reason should be considered as a novel therapeutic target for AD.
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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.