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Liviu Aron

Researcher at Harvard University

Publications -  19
Citations -  2469

Liviu Aron is an academic researcher from Harvard University. The author has contributed to research in topics: Retinal degeneration & Retinitis pigmentosa. The author has an hindex of 14, co-authored 19 publications receiving 1945 citations. Previous affiliations of Liviu Aron include Max Planck Society.

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The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4

TL;DR: This work mapped the critical region for senescence-induced activity and identified the transcriptional regulator responsible for this regulation, GATA4, previously known as a regulator of embryonic development, which affects senescent cells and their microenvironment and suggests the existence of an independent senescENCE regulatory network that controls the SASP.
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REST and stress resistance in ageing and Alzheimer’s disease

TL;DR: It is shown that induction of the repressor element 1-silencing transcription factor (REST) is a universal feature of normal ageing in human cortical and hippocampal neurons, and levels during ageing are closely correlated with cognitive preservation and longevity.
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TBK1 Suppresses RIPK1-Driven Apoptosis and Inflammation during Development and in Aging

TL;DR: It is shown that in Tbk1+/- mice, the reduced myeloid TAK1 expression promotes all the key hallmarks of ALS/FTD, including neuroinflammation, TDP-43 aggregation, axonal degeneration, neuronal loss, and behavior deficits, which are blocked upon inhibition of RIPK1.
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Absence of Ret signaling in mice causes progressive and late degeneration of the nigrostriatal system.

TL;DR: It is found that Ret, but not TrkB, ablation causes progressive and adult-onset loss of DA neurons specifically in the substantia nigra pars compacta, degeneration of DA nerve terminals in striatum, and pronounced glial activation.
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Regulation of lifespan by neural excitation and REST

TL;DR: It is shown that extended longevity in humans is associated with a distinct transcriptome signature in the cerebral cortex that is characterized by downregulation of genes related to neural excitation and synaptic function, which reveals a conserved mechanism of ageing that is mediated by neural circuit activity and regulated by REST.