Mitophagy in Alzheimer's Disease and Other Age-Related Neurodegenerative Diseases.
Qian Cai,Yu Young Jeong +1 more
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TLDR
The molecular mechanisms underlying mitophagy defects in Alzheimer’s disease and other age-related neurodegenerative diseases, as well as the therapeutic potential ofMitophagy-enhancing strategies to combat these disorders are discussed.Citations
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Induction of autophagy by spermidine promotes longevity
Tobias Eisenberg,Heide Knauer,Alexandra Schauer,Sabrina Büttner,Christoph Ruckenstuhl,Didac Carmona-Gutierrez,Julia Ring,Sabrina Schroeder,Christoph Magnes,Lucia Antonacci,Heike Fussi,Luiza Deszcz,Luiza Deszcz,Regina Hartl,Regina Hartl,Elisabeth Schraml,Alfredo Criollo,Evgenia Megalou,Daniela Weiskopf,Peter Laun,Gino Heeren,Michael Breitenbach,Beatrix Grubeck-Loebenstein,Eva Herker,Birthe Fahrenkrog,Kai-Uwe Fröhlich,Frank Sinner,Nektarios Tavernarakis,Nadège Minois,Nadège Minois,Nadège Minois,Guido Kroemer,Frank Madeo +32 more
TL;DR: Administration of spermidine markedly extended the lifespan of yeast, flies and worms, and human immune cells and inhibited oxidative stress in ageing mice, and found that enhanced autophagy is crucial for polyamine-induced suppression of necrosis and enhanced longevity.
Journal ArticleDOI
Mitochondrial Dysfunction and Oxidative Stress in Alzheimer's Disease.
TL;DR: In this paper, the authors focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of Alzheimer's disease, emphasizing a framework of existing and potential therapeutic approaches.
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Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria.
Albin John,P. Hemachandra Reddy +1 more
TL;DR: The mechanisms of synaptic action, mitochondrial regulation/dysregulation, resulting synaptic changes caused by amyloid beta and phosphorylated tau in AD progression and impairments in LTD and reactivation of microglia are discussed.
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Defective mitophagy in Alzheimer's disease.
TL;DR: Whether a partial reduction of Drp1 can be aMitophagy enhancer and a therapeutic target for mitophagy in AD and other neurological diseases is discussed.
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Regulation of Mammalian Mitochondrial Dynamics: Opportunities and Challenges.
TL;DR: This review describes recent insights into the potential molecular mechanisms underlying mitochondrial fusion and fission, particularly highlighting the coordinating roles of different mitochondria-shaping proteins in the processes, as well as the roles of the endoplasmic reticulum, the actin cytoskeleton and membrane phospholipids in the regulation of mitochondrial dynamics.
References
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Oxidants, oxidative stress and the biology of ageing.
Toren Finkel,Nikki J. Holbrook +1 more
TL;DR: Evidence that the appropriate and inappropriate production of oxidants, together with the ability of organisms to respond to oxidative stress, is intricately connected to ageing and life span is reviewed.
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Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Michael T. Lin,M. Flint Beal +1 more
TL;DR: Treatments targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria hold great promise in ageing-related neurodegenerative diseases.
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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
Tohru Kitada,Shuichi Asakawa,Nobutaka Hattori,Hiroto Matsumine,Yasuhiro Yamamura,Shinsei Minoshima,Masayuki Yokochi,Yoshikuni Mizuno,Nobuyoshi Shimizu +8 more
TL;DR: Mutations in the newly identified gene appear to be responsible for the pathogenesis of Autosomal recessive juvenile parkinsonism, and the protein product is named ‘Parkin’.
Journal ArticleDOI
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
Journal ArticleDOI
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Eriza Maria Valente,Patrick M. Abou-Sleiman,Viviana Caputo,Miratul M. K. Muqit,Kirsten Harvey,Suzana Gispert,Zeeshan Ali,Domenico Del Turco,Anna Rita Bentivoglio,Daniel G. Healy,Alberto Albanese,Robert L. Nussbaum,Rafael González-Maldonado,Thomas Deller,S Salvi,Pietro Cortelli,William P. Gilks,David S. Latchman,Roberk J. Harvey,Bruno Dallapiccola,Georg Auburger,Nicholas W. Wood +21 more
TL;DR: The identification of two homozygous mutations affecting the PINK1 kinase domain in three consanguineous PARK6 families provide a direct molecular link between mitochondria and the pathogenesis of PD.
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