ArticleAlzheimer's research & therapy2019
Peripheral administration of human recombinant ApoJ/clusterin modulates brain beta-amyloid levels in APP23 mice.
Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- Combating ageing beyond the cell: Emerging roles of extracellular proteostasis.The FEBS journal · 2026Review
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- Mechanisms, Mediators, and Pharmacological Approaches Targeting Brain Cholesterol Transport in Alzheimer's Disease.Current pharmaceutical design · 2026Review
- Mechanisms of high-density lipoprotein in regulating blood-brain barrier function: insights and implications.Fluids and barriers of the CNS · 2025Review
- Intrahippocampally Injected Human Recombinant Clusterin Reduces Amyloid-β Aggregate Size in Cerebral Arteriole Walls of Clusterin Knockout Mice.Neuropathology and applied neurobiology · 2025Article
- Bridging systemic metabolic dysfunction and Alzheimer's disease: the liver interface.Molecular neurodegeneration · 2025Review
- Clusterin: structure, function and roles in disease.International journal of medical sciences · 2025Review
- Discovery of a small molecule secreted clusterin enhancer that improves memory in Alzheimer's disease mice.npj drug discovery · 2025Article
- Potential of molecular chaperones for treating Alzheimer's disease.Neural regeneration research · 2024Article
- The presence of circulating human apolipoprotein J reduces the occurrence of cerebral microbleeds in a transgenic mouse model with cerebral amyloid angiopathy.Alzheimer's research & therapy · 2024Article
- Effects of Intravenously Administered Plasma from Exercise-Trained Donors on Microglia and Cytokines in a Transgenic Rat Model of Alzheimer's Disease.Brain plasticity (Amsterdam, Netherlands) · 2024Article
- Extracellular protein homeostasis in neurodegenerative diseases.Nature reviews. Neurology · 2023Review
- Recent advances on the molecular mechanisms of exercise-induced improvements of cognitive dysfunction.Translational neurodegeneration · 2023Review
- The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Clusterin negatively modulates mechanical stress-mediated ligamentum flavum hypertrophy through TGF-β1 signaling.Experimental & molecular medicine · 2022Article
- The Roles of Fatty Acids and Apolipoproteins in the Kidneys.Metabolites · 2022Review
- Endogenous Human Proteins Interfering with Amyloid Formation.Biomolecules · 2022Review
- HDL Accessory Proteins in Parkinson's Disease-Focusing on Clusterin (Apolipoprotein J) in Regard to Its Involvement in Pathology and Diagnostics-A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Functional insight into LOAD-associated microglial response genes.Open biology · 2022Review
- Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundApoJ/clusterin is a multifunctional protein highly expressed in the brain. The implication of ApoJ in β-amyloid (Aβ) fibrillization and clearance in the context of Alzheimer's disease has been widely studied, although the source and concentration of ApoJ that promotes or inhibits Aβ cerebral accumulation is not clear yet. ApoJ is abundant in plasma and approximately 20% can appear bound to HDL-particles. In this regard, the impact of plasmatic ApoJ and its lipidation status on cerebral β-amyloidosis is still not known. Hence, our main objective was to study the effect of a peripheral increase of free ApoJ or reconstituted HDL particles containing ApoJ in an experimental model of cerebral β-amyloidosis.
methodsFourteen-month-old APP23 transgenic mice were subjected to subchronic intravenous treatment with rHDL-rApoJ nanodiscs or free rApoJ for 1 month. Aβ concentration and distribution in the brain, as well as Aβ levels in plasma and CSF, were determined after treatments. Other features associated to AD pathology, such as neuronal loss and neuroinflammation, were also evaluated.
resultsBoth ApoJ-based treatments prevented the Aβ accumulation in cerebral arteries and induced a decrease in total brain insoluble Aβ
conclusionsOur results demonstrate that an increase in circulating human rApoJ induces a reduction of insoluble Aβ and CAA load in the brain of APP23 mice. Thus, our study suggests that peripheral interventions, based on treatments with multifunctional physiological chaperones, offer therapeutic opportunities to regulate the cerebral Aβ load.
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