ArticlePloS one2015
Lysosomal Enzyme Glucocerebrosidase Protects against Aβ1-42 Oligomer-Induced Neurotoxicity.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Taliglucerase Alfa Reduces Amyloid-β Burden by Restoring Autophagic Pathways in a Neuronal Model of Alzheimer's Disease.Neurochemical research · 2026Article
- Therapeutic Modulation of the Nox2-Hv1-ROS Axis by Botulinum Neurotoxin A Confers Protection Against CoClInternational journal of molecular sciences · 2025Article
- Cell-specific protein expression in Alzheimer's disease prefrontal cortex.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Cerium-doped Prussian blue biomimetic nanozyme as an amplified pyroptosis inhibitor mitigate Aβ oligomer-induced neurotoxicity in Alzheimer's disease.Journal of nanobiotechnology · 2025Article
- Article
- Endolysosomal impairment by binding of amyloid beta or MAPT/Tau to V-ATPase and rescue via the HYAL-CD44 axis in Alzheimer disease.Autophagy · 2023Article
- Impact of GBA variants on longitudinal freezing of gait progression in early Parkinson's disease.Journal of neurology · 2023Article
- Live imaging of intra-lysosome pH in cell lines and primary neuronal culture using a novel genetically encoded biosensor.Autophagy · 2021Article
- Endolysosome and Autolysosome Dysfunction in Alzheimer's Disease: Where Intracellular and Extracellular Meet.CNS drugs · 2019Review
- Candidate-based screening via gene modulation in human neurons and astrocytes implicates FERMT2 in Aβ and TAU proteostasis.Human molecular genetics · 2019Article
- D409H GBA1 mutation accelerates the progression of pathology in A53T α-synuclein transgenic mouse model.Acta neuropathologica communications · 2018Article
- α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism.Molecular neurodegeneration · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Glucocerebrosidase (GCase) functions as a lysosomal enzyme and its mutations are known to be related to many neurodegenerative diseases, including Gaucher's disease (GD), Parkinson's disease (PD), and Dementia with Lewy Bodies (DLB). However, there is little information about the role of GCase in the pathogenesis of Alzheimer's disease (AD). Here we demonstrate that GCase protein levels and enzyme activity are significantly decreased in sporadic AD. Moreover, Aβ1-42 oligomer treatment results in neuronal cell death that is concomitant with decreased GCase protein levels and enzyme activity, as well as impairment in lysosomal biogenesis and acidification. Importantly, overexpression of GCase promotes the lysosomal degradation of Aβ1-42 oligomers, restores the lysosomal impairment, and protects against the toxicity in neurons treated with Aβ1-42 oligomers. Our findings indicate that a deficiency of GCase could be involved in progression of AD pathology and suggest that augmentation of GCase activity may be a potential therapeutic option for the treatment of AD.
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Registered trials
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