ArticleLife sciences2012
Endolysosome involvement in LDL cholesterol-induced Alzheimer's disease-like pathology in primary cultured neurons.
Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026Review
- LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models.Journal of neurochemistry · 2026Article
- Lysosomal membrane homeostasis and its importance in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- LDL Exposure Disrupts Mitochondrial Function and Dynamics in a Hippocampal Neuronal Cell Line.Molecular neurobiology · 2025Article
- Calcium signaling from damaged lysosomes induces cytoprotective stress granules.The EMBO journal · 2024Article
- Involvement of Endolysosomes and Aurora Kinase A in the Regulation of Amyloid β Protein Levels in Neurons.International journal of molecular sciences · 2024Article
- HERV-K (HML-2) Envelope Protein Induces Mitochondrial Depolarization and Neurotoxicity via Endolysosome Iron Dyshomeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- A mechanism that transduces lysosomal damage signals to stress granule formation for cell survival.bioRxiv : the preprint server for biology · 2024Article
- Weak base drug-induced endolysosome iron dyshomeostasis controls the generation of reactive oxygen species, mitochondrial depolarization, and cytotoxicity.NeuroImmune pharmacology and therapeutics · 2024Article
- Modulatory Effect of Blood LDL Cholesterol on the Association between Cerebral Aβ and Tau Deposition in Older Adults.The journal of prevention of Alzheimer's disease · 2024Article
- Mu opioid receptor-mediated release of endolysosome iron increases levels of mitochondrial iron, reactive oxygen species, and cell death.NeuroImmune pharmacology and therapeutics · 2023Article
- Heterogeneity of ferrous iron-containing endolysosomes and effects of endolysosome iron on endolysosome numbers, sizes, and localization patterns.Journal of neurochemistry · 2022Article
- Lysosomal Stress Response (LSR): Physiological Importance and Pathological Relevance.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- Antiretroviral Drugs Promote Amyloidogenesis by De-Acidifying Endolysosomes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Dynamic Changes in the Levels of Amyloid-βFrontiers in molecular neuroscience · 2021Article
- Intra-gastrointestinal amyloid-β1-42 oligomers perturb enteric function and induce Alzheimer's disease pathology.The Journal of physiology · 2020Article
- Role of endolysosomes and inter-organellar signaling in brain disease.Neurobiology of disease · 2020Review
- Role of endolysosomes and pH in the pathogenesis and treatment of glioblastoma.Cancer reports (Hoboken, N.J.) · 2019Article
- Importance of measuring endolysosome, cytosolic, and extracellular pH in understanding the pathogenesis of and possible treatments for glioblastoma multiforme.Cancer reports (Hoboken, N.J.) · 2019Article
- Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: A role for the LDL receptor and cholesterol metabolism in adult neural precursor cells.Molecular metabolism · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
aimsElevated levels of circulating cholesterol are extrinsic factors contributing to the pathogenesis of sporadic Alzheimer's disease (AD). We showed previously that rabbits fed a cholesterol-enriched diet exhibited blood-brain barrier (BBB) dysfunction, increased accumulation of apolipoprotein B (ApoB) in brain neurons, and endolysosomes in brain had disturbed structures and functions. These effects were linked to increased amyloid beta (Aβ) production, increased tau-pathology, and disrupted synaptic integrity. Because pathological changes to endolysosomes represent a very early event in sporadic AD, we determined here the extent to which ApoB-containing LDL cholesterol altered the structure and function of endolysosomes and contributed to the development of AD-like pathology in primary cultured neurons. MAIN
methodsCholesterol distribution and endolysosome morphology were determined histologically. Endolysosome pH was measured ratio-metrically with LysoSensor dye. Endolysosome enzyme activity was measured for acid phosphatase, cathepsins B and D, and beta-site APP cleaving enzyme 1 (BACE-1). AD-like pathologies, including increased production of Aβ, increased tau-pathology, and disrupted synaptic integrity were determined using ELISA, immunoblotting, and immunostaining techniques. KEY
findingsTreatment of neurons with ApoB-containing LDL cholesterol increased endolysosome accumulation of cholesterol, enlarged endolysosomes, and elevated endolysosome pH. In addition, ApoB-containing LDL cholesterol increased endolysosome accumulation of BACE-1, enhanced BACE-1 activity, increased Aβ levels, increased levels of phosphorylated tau, and decreased levels of synaptophysin. SIGNIFICANCE: Our findings suggest strongly that alterations in the structure and function of endolysosomes play a key role in the exhibition of pathological features of AD that result from neuronal exposure to ApoB-containing LDL cholesterol.
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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.