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pubmed, article, google, scholar, disease, parkinsons, central, autophagy, cas, lrrk, lysosomal, gba, cell, cells, glucocerebrosidase, patients, mutations, mtor, macrophages, usenko, gene, httpsdoiorgs, parkinson, levels, dysfunction, mutation, dis, regulation, bezrukova, emelyanov, alphasynuclein, peripheral, activity, biol, neurosci, analysis, data, basharova, pathogenesis, blood, access, study, res, neurol, brain, biochem, parkinsonism, mol, privacy, cookies,

Topics {✒️}

month download article/chapter primary patient-derived macrophages elevated extracellular α-synuclein extracellular vesicle-mediated spread chaperone-mediated-autophagy deficiency ipsc-derived dopamine neurons pbmc-derived macrophages carboxy-terminally truncated species patient-derived cell cultures gtpase-p38 mapk signaling huntingtin-induced cell death 4e-bp1 pathways leading full article pdf treating lrrk2-related parkinson monocyte-derived macrophages nikolaev ma references aharon-peretz common lrrk2 mutation mtor-mediated s6k1 privacy choices/manage cookies alpha-synuclein protein disease ipsc-neuronal cells potential binding sites migdalska-richards α-synuclein form alpha-synuclein pathology alpha-synuclein nitration potential treatment approaches decreased p62 levels steady-state autophagy autophagy-related proteins g2019s-lrrk2-pd patients torc-specific phosphorylation peripheral blood cells evident lysosomal dysfunction pharmacological chaperone ncgc00241607 competing financial interests macrophages derived studying glucocerebrosidase dysfunction mtor signaling pathway altered ceramide metabolism nrc «kurchatov institute» including phosphorylated mtor direct mtor dysregulation mtor-regulated pathways mtor-independent pathways gba1 rodent models autophagy-lysosome system autophagy-lysosomal pathway holds exclusive rights

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         headline:Autophagy Process in Parkinson’s Disease Depends on Mutations in the GBA1 and LRRK2 Genes
         description:Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and abnormal aggregation of the alpha-synuclein protein. Disruption of the autophagy-lysosomal pathway is closely associated with PD pathogenesis. Here, using western-blot analysis we assessed the level of autophagy-related proteins, including phosphorylated mTOR (p-mTOR), phosphorylated RPS6 (p-RPS6), beclin-1 (BECN1), LC3B, p62, and cathepsin D (CTSD) in macrophages derived from peripheral blood mononuclear cells (PBMC-derived macrophages) of GBA1-PD (p.N370S/N, p.L444P/N), LRRK2-PD (p.G2019S/N), idiopathic PD (iPD) patients, and healthy controls. Our findings revealed mutation-specific disruptions in autophagy pathways among PD patients. In p.N370S-GBA1-PD, PBMC-derived macrophages exhibited elevated levels of p-RPS6, BECN1, LC3B-II and decreased mature form of CTSD levels suggesting more active mTOR-dependent autophagy initiation alongside potential autophagosome accumulation that may lead to downregulation of lysosomal degradation. p.L444P-GBA1-PD PBMC-derived macrophages showed increased levels of p-RPS6 and BECN1, coupled with decreased p62 levels and stable mature form of CTSD and LC3B-II, indicative of enhanced autophagy flux driven by mTOR activity without evident lysosomal dysfunction. In p.G2019S-LRRK2-PD patients, PBMC-derived macrophages demonstrated elevated p-RPS6, LC3B-II, and mature CTSD levels, alongside reduced p62 levels. These changes suggest higher basal autophagosome abundance in steady-state autophagy and turnover, potentially driven by lysosomal alterations rather than direct mTOR dysregulation. These mutation-dependent differences highlight distinct autophagy dynamics in GBA1-PD and LRRK2-PD, underscoring the critical role of genetic mutations in modulating PD pathogenesis. Our results emphasize the necessity for subtype-specific therapeutic strategies targeting autophagy and other mTOR-regulated pathways to address the heterogeneity of PD mechanisms.
         datePublished:2025-05-19T00:00:00Z
         dateModified:2025-05-19T00:00:00Z
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      headline:Autophagy Process in Parkinson’s Disease Depends on Mutations in the GBA1 and LRRK2 Genes
      description:Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and abnormal aggregation of the alpha-synuclein protein. Disruption of the autophagy-lysosomal pathway is closely associated with PD pathogenesis. Here, using western-blot analysis we assessed the level of autophagy-related proteins, including phosphorylated mTOR (p-mTOR), phosphorylated RPS6 (p-RPS6), beclin-1 (BECN1), LC3B, p62, and cathepsin D (CTSD) in macrophages derived from peripheral blood mononuclear cells (PBMC-derived macrophages) of GBA1-PD (p.N370S/N, p.L444P/N), LRRK2-PD (p.G2019S/N), idiopathic PD (iPD) patients, and healthy controls. Our findings revealed mutation-specific disruptions in autophagy pathways among PD patients. In p.N370S-GBA1-PD, PBMC-derived macrophages exhibited elevated levels of p-RPS6, BECN1, LC3B-II and decreased mature form of CTSD levels suggesting more active mTOR-dependent autophagy initiation alongside potential autophagosome accumulation that may lead to downregulation of lysosomal degradation. p.L444P-GBA1-PD PBMC-derived macrophages showed increased levels of p-RPS6 and BECN1, coupled with decreased p62 levels and stable mature form of CTSD and LC3B-II, indicative of enhanced autophagy flux driven by mTOR activity without evident lysosomal dysfunction. In p.G2019S-LRRK2-PD patients, PBMC-derived macrophages demonstrated elevated p-RPS6, LC3B-II, and mature CTSD levels, alongside reduced p62 levels. These changes suggest higher basal autophagosome abundance in steady-state autophagy and turnover, potentially driven by lysosomal alterations rather than direct mTOR dysregulation. These mutation-dependent differences highlight distinct autophagy dynamics in GBA1-PD and LRRK2-PD, underscoring the critical role of genetic mutations in modulating PD pathogenesis. Our results emphasize the necessity for subtype-specific therapeutic strategies targeting autophagy and other mTOR-regulated pathways to address the heterogeneity of PD mechanisms.
      datePublished:2025-05-19T00:00:00Z
      dateModified:2025-05-19T00:00:00Z
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      pageEnd:18
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         Parkinson’s disease
          GBA1
          LRRK2
         PBMC-derived macrophages
         mTOR
         Autophagy
         Human Genetics
         Biochemistry
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         Zoology
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