Mitostasis in Neurons: Maintaining Mitochondria in an Extended Cellular Architecture
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TLDR
Both long-range transport and local processing are at work in achieving neuronal mitostasis-the maintenance of an appropriately distributed pool of healthy mitochondria for the duration of a neuron's life.About:
This article is published in Neuron.The article was published on 2017-11-01 and is currently open access. It has received 334 citations till now. The article focuses on the topics: Mitophagy & Mitochondrial fission.read more
Citations
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Journal ArticleDOI
Selective neuronal vulnerability in Parkinson disease.
TL;DR: The evidence for and against the spreading LP model are discussed, as well as evidence that cell-autonomous factors govern both α-syn pathology and neuronal death.
Journal ArticleDOI
Microglia monitor and protect neuronal function through specialized somatic purinergic junctions
Csaba Cserép,Balázs Pósfai,Nikolett Lénárt,Rebeka Fekete,Zsófia I. László,Zsolt Lele,Barbara Orsolits,Gábor Molnár,Steffanie Heindl,Anett D. Schwarcz,Katinka Ujvári,Zsuzsanna Környei,Krisztina Tóth,Eszter Szabadits,Beáta Sperlágh,Mária Baranyi,László Csiba,Tibor Hortobágyi,Tibor Hortobágyi,Tibor Hortobágyi,Zsófia Maglóczky,Bernadett Martinecz,Gábor Szabó,Ferenc Erdélyi,Róbert Szipőcs,Michael M. Tamkun,Benno Gesierich,Marco Duering,István Katona,Arthur Liesz,Gábor Tamás,Adam Denes +31 more
TL;DR: The junctions appear to provide a major site for microglia-neuron communication and may help to mediate the neuroprotective effects ofmicroglia after acute brain injury, and microglial processes at these junctions could potentially monitor and protect neuronal functions.
Journal ArticleDOI
PINK1 and Parkin mitochondrial quality control: a source of regional vulnerability in Parkinson’s disease
TL;DR: This review focuses on understanding the unique challenges faced by the mitochondria in neurons vulnerable to neurodegeneration in Parkinson’s and summarizes evidence that mitochondrial dysfunction contributes to disease pathogenesis and to cell death in these subpopulations.
Book ChapterDOI
Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.
Carlotta Giorgi,Saverio Marchi,Ines C.M. Simoes,Ziyu Ren,Giampaolo Morciano,Mariasole Perrone,Paulina Patalas-Krawczyk,Sabine Borchard,Paulina Jędrak,Karolina Pierzynowska,Jędrzej Szymański,David Q.-H. Wang,Piero Portincasa,Grzegorz Węgrzyn,Hans Zischka,Pawel Dobrzyn,Massimo Bonora,Jerzy Duszyński,Alessandro Rimessi,Agnieszka Karkucinska-Wieckowska,Agnieszka Dobrzyn,Gyorgy Szabadkai,Barbara Zavan,Paulo J. Oliveira,Vilma A. Sardão,Paolo Pinton,Mariusz R. Wieckowski +26 more
TL;DR: An update regarding the key roles of ROS-mitochondria cross talk in different fundamental physiological or pathological situations accompanying aging is provided, highlighting that mitochondrial ROS may be a decisive target in clinical practice.
Journal ArticleDOI
Axonal transport: Driving synaptic function
TL;DR: Improved and complementary in vitro and in vivo imaging approaches are allowing the elucidation of increasingly intricate mechanisms by which the activities of dynein and kinesin motors regulate organelle transport along axons, which will provide a framework for the design of successful therapeutic interventions for both genetic and trauma-induced disruptions.
References
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Journal ArticleDOI
An Energy Budget for Signaling in the Grey Matter of the Brain
David Attwell,Simon B. Laughlin +1 more
TL;DR: The estimates of energy usage predict the use of distributed codes, with ≤15% of neurons simultaneously active, to reduce energy consumption and allow greater computing power from a fixed number of neurons.
Journal ArticleDOI
Protein degradation and protection against misfolded or damaged proteins
TL;DR: A full understanding of the pathogenesis of the protein-folding diseases will require greater knowledge of how misfolded proteins are recognized and selectively degraded.
Journal ArticleDOI
The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy
Michael Lazarou,Danielle A. Sliter,Lesley A. Kane,Shireen A. Sarraf,Chunxin Wang,Jonathon L. Burman,Dionisia P. Sideris,Adam I. Fogel,Richard J. Youle +8 more
TL;DR: Using genome editing to knockout five autophagy receptors in HeLa cells, this work shows that two receptors previously linked to xenophagy, NDP52 and optineurin, are the primary receptors for PINK1- and parkin-mediated mitophagy.
Journal ArticleDOI
Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin.
Ira E. Clark,Mark W. Dodson,Changan Jiang,Joseph Cao,Jun R. Huh,Jae Hong Seol,Soon Ji Yoo,Bruce A. Hay,Ming Guo +8 more
TL;DR: Removal of Drosophila PINK1 homologue function results in male sterility, apoptotic muscle degeneration, defects in mitochondrial morphology and increased sensitivity to multiple stresses including oxidative stress, which underscores the importance of mitochondrial dysfunction as a central mechanism of Parkinson's disease pathogenesis.
Journal ArticleDOI
Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
Jeehye Park,Sung Bae Lee,Sungkyu Lee,Yongsung Kim,Saera Song,Sunhong Kim,Eunkyung Bae,Jaeseob Kim,Minho Shong,Jin Man Kim,Jongkyeong Chung +10 more
TL;DR: The genetic evidence clearly establishes that Parkin and PINK1 act in a common pathway in maintaining mitochondrial integrity and function in both muscles and dopaminergic neurons.
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