2025
An integrative systems-biology approach defines mechanisms of Alzheimer’s disease neurodegeneration
Leventhal M, Zanella C, Kang B, Peng J, Gritsch D, Liao Z, Bukhari H, Wang T, Pao P, Danquah S, Benetatos J, Nehme R, Farhi S, Tsai L, Dong X, Scherzer C, Feany M, Fraenkel E. An integrative systems-biology approach defines mechanisms of Alzheimer’s disease neurodegeneration. Nature Communications 2025, 16: 4441. PMID: 40393985, PMCID: PMC12092734, DOI: 10.1038/s41467-025-59654-w.Peer-Reviewed Original ResearchConceptsDisease proteomicsDrosophila model of Alzheimer's diseaseAlzheimer's diseaseDisease neurodegenerationSystems-biology approachAlzheimer's disease neurodegenerationModel of Alzheimer's diseaseModify gene expressionAge-associated neurodegenerationDrosophila modelTau proteinGenetic screeningGenetic variantsGene expressionRelevant pathwaysDNA damageAmeliorate neurodegenerationDrosophilaYears of intensive investigationNeural progenitor cellsProteomicsNeurodegenerationNeuronal deathAlzheimerProgenitor cellsInhibition of amyloid beta oligomer accumulation by NU-9: A unifying mechanism for the treatment of neurodegenerative diseases
Johnson E, Nowar R, Viola K, Huang W, Zhou S, Bicca M, Zhu W, Kranz D, Klein W, Silverman R. Inhibition of amyloid beta oligomer accumulation by NU-9: A unifying mechanism for the treatment of neurodegenerative diseases. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2402117122. PMID: 40030015, PMCID: PMC11912461, DOI: 10.1073/pnas.2402117122.Peer-Reviewed Original ResearchConceptsProtein aggregationNeurodegenerative diseasesMechanisms of protein aggregationAmyloid-beta oligomersAlzheimer's disease neurodegenerationEndolysosomal traffickingBeta oligomersOligomer accumulationTreatment of neurodegenerative diseasesTDP-43Disease neurodegenerationPeptide aggregationLysosome-dependentCathepsin LProteinHippocampal neuronsPathological accumulationQuantitative assayTraffickingCellular mechanismsCathepsin BBlock neurodegenerationImmunofluorescence imagingPathogenic mechanismsNeurodegeneration
2000
Neuromelanin biosynthesis is driven by excess cytosolic catecholamines not accumulated by synaptic vesicles
Sulzer D, Bogulavsky J, Larsen K, Behr G, Karatekin E, Kleinman M, Turro N, Krantz D, Edwards R, Greene L, Zecca L. Neuromelanin biosynthesis is driven by excess cytosolic catecholamines not accumulated by synaptic vesicles. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 11869-11874. PMID: 11050221, PMCID: PMC17261, DOI: 10.1073/pnas.97.22.11869.Peer-Reviewed Original ResearchConceptsCytosolic catecholaminesSubstantia nigraDisease neurodegenerationCytosolic dopamineRat substantia nigraSynaptic vesiclesParkinson's disease neurodegenerationHuman substantia nigraIron chelator desferrioxamineCatecholamine neuronsFunction of neuromelaninDeep brain regionsParkinson's diseaseAdenoviral-mediated overexpressionBrain regionsDouble-membrane autophagic vacuolesVesicular accumulationPC12 cell culturesChelator desferrioxamineDopamineNM granulesAntioxidant mechanismsPC12 cellsNeuromelaninNeurite outgrowth
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