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Signaling interactions among neurons impact cell fitness and death in Alzheimer's disease

Neural Regeneration Research 2023年第4期18卷 784-789页

作者： catherine yeates Prajakta Deshpande Madhuri Kango-Singh Amit Singh Department of Biology University of DaytonDaytonOHUSA Premedical Program University of DaytonDaytonOHUSA Center for Tissue Regeneration and Engineering at Dayton(TREND) University of DaytonDaytonOHUSA The Integrative Science and Engineering Center University of DaytonDaytonOHUSA Center for Genomic Advocacy(TCGA) Indiana State UniversityTerre HauteINUSA

The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are *** the preclinical period,homeostatic mechanisms may help prevent widespread cell *** has pointed towards selective cell death of diseased neurons playing a potentially protective *** the disease progresses,dysregulation of signaling pathways that govern cell death contributes to *** activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated *** mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type *** review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type *** competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal *** clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying *** genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s *** approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.

关键词： Alzheimer’s disease amyloid-beta 42 mediated neurodegeneration cell competition Drosophila c-Jun N-terminal kinase signaling suboptimal cell super competition super competitor cell two clone-approach wild type cell

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