ArticleNeuropathology and applied neurobiology2020
Significance of cytosolic cathepsin D in Alzheimer's disease pathology: Protective cellular effects of PLGA nanoparticles against β-amyloid-toxicity.
Article in Neuropathology and applied neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Attenuation of Tau-Mediated β-Amyloid1-42 Aggregation by Native PLGA Nanoparticles and Its Relevance to Alzheimer Disease Pathology.International journal of molecular sciences · 2026Article
- Zinc-mediated lysosomal activation by 1H10 enhances autophagy and attenuates tau pathology in Alzheimer's disease models.Molecular brain · 2026Article
- Lysosome-Acidifying Nanoparticles Rescue A30P α-Synuclein Induced Neuronal Death in Cellular and Drosophila Models of Parkinson's Disease.Advanced healthcare materials · 2026Article
- Native PLGA nanoparticles attenuate disease pathology via multiple pathways in 5xFAD Alzheimer's model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Amylin exacerbates tau pathology in the visual cortex of diabetic mice by impairing lysosomal activity.Genes & diseases · 2025Article
- Rescuing lysosomal/autophagic defects via nanoapproach: implications for lysosomal/autophagic defect-related diseases.Journal of Zhejiang University. Science. B · 2025Review
- Temperature-Dependent Aggregation of Tau Protein Is Attenuated by Native PLGA Nanoparticles Under in vitro Conditions.International journal of nanomedicine · 2025Article
- Polymers for the treatment of Alzheimer's disease.Frontiers in pharmacology · 2025Review
- New preclinical biomarkers for prion diseases in the cerebrospinal fluid proteome revealed by mass spectrometry.The veterinary quarterly · 2024Article
- Native PLGA nanoparticles attenuate Aβ-seed induced tau aggregation under in vitro conditions: potential implication in Alzheimer's disease pathology.Scientific reports · 2024Article
- Detection of β-amyloid aggregates/plaques in 5xFAD mice by labelled native PLGA nanoparticles: implication in the diagnosis of alzheimer's disease.Journal of nanobiotechnology · 2023Article
- Advancements in high-resolution 3D microscopy analysis of endosomal morphology in postmortem Alzheimer's disease brains.Frontiers in neuroscience · 2023Article
- Significance of native PLGA nanoparticles in the treatment of Alzheimer's disease pathology.Bioactive materials · 2022Article
- Impairment of the autophagy-lysosomal pathway in Alzheimer's diseases: Pathogenic mechanisms and therapeutic potential.Acta pharmaceutica Sinica. B · 2022Review
- Unconjugated PLGA nanoparticles attenuate temperature-dependent β-amyloid aggregation and protect neurons against toxicity: implications for Alzheimer's disease pathology.Journal of nanobiotechnology · 2022Article
- Implications of exosomes derived from cholesterol-accumulated astrocytes in Alzheimer's disease pathology.Disease models & mechanisms · 2021Article
- Cathepsin D-Managing the Delicate Balance.Pharmaceutics · 2021Review
- The Other Side of Alzheimer's Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers.Journal of personalized medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEvidence suggests that amyloid β (Aβ) peptides play an important role in the degeneration of neurons during the development of Alzheimer's disease (AD), the prevalent cause of dementia affecting the elderly. The endosomal-lysosomal system, which acts as a major site for Aβ metabolism, has been shown to exhibit abnormalities in vulnerable neurons of the AD brain, reflected by enhanced levels/expression of lysosomal enzymes including cathepsin D (CatD). At present, the implication of CatD in selective neuronal vulnerability in AD pathology remains unclear.
methodsWe evaluated the role of CatD in the degeneration of neurons in Aβ-treated cultures, transgenic AD mouse model (that is 5xFAD) and post mortem AD brain samples.
resultsOur results showed that Aβ
conclusionOur study reveals that increased cytosolic level/activity of CatD play an important role in determining neuronal vulnerability in AD. Additionally, native PLGA can protect neurons against Aβ toxicity by restoring lysosomal membrane integrity, thus signifying its implication in attenuating AD.
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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.