Astrocytes in Neurodegenerative Disease: Table 1. DOI Open Access
Hemali Phatnani, Tom Maniatis

Cold Spring Harbor Perspectives in Biology, Journal Year: 2015, Volume and Issue: 7(6), P. a020628 - a020628

Published: April 15, 2015

Hemali Phatnani and Tom Maniatis Columbia University Medical Center, Department of Biochemistry Molecular Biophysics, New York, York 10032 Correspondence: tm2472{at}columbia.edu

Language: Английский

Mitochondria: In Sickness and in Health DOI Creative Commons
Jodi Nunnari, Anu Suomalainen

Cell, Journal Year: 2012, Volume and Issue: 148(6), P. 1145 - 1159

Published: March 1, 2012

Language: Английский

Citations

2939

Physiological Roles of Mitochondrial Reactive Oxygen Species DOI Creative Commons
Laura A. Sena, Navdeep S. Chandel

Molecular Cell, Journal Year: 2012, Volume and Issue: 48(2), P. 158 - 167

Published: Oct. 1, 2012

Language: Английский

Citations

2337

Mitochondrial form and function DOI
Jonathan R. Friedman, Jodi Nunnari

Nature, Journal Year: 2014, Volume and Issue: 505(7483), P. 335 - 343

Published: Jan. 14, 2014

Language: Английский

Citations

1576

PINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial Motility DOI Creative Commons
Xinnan Wang, Dominic Winter, Ghazaleh Ashrafi

et al.

Cell, Journal Year: 2011, Volume and Issue: 147(4), P. 893 - 906

Published: Nov. 1, 2011

Language: Английский

Citations

1103

13 reasons why the brain is susceptible to oxidative stress DOI Creative Commons
James N. Cobley,

Maria Luisa Fiorello,

Damian M. Bailey

et al.

Redox Biology, Journal Year: 2018, Volume and Issue: 15, P. 490 - 503

Published: Feb. 3, 2018

The human brain consumes 20% of the total basal oxygen (O2) budget to support ATP intensive neuronal activity. Without sufficient O2 demands, activity fails, such that, even transient ischemia is neurodegenerative. While essentiality function clear, how oxidative stress causes neurodegeneration ambiguous. Ambiguity exists because many reasons why susceptible remain obscure. Many are erroneously understood as deleterious result adventitious derived free radical and non-radical species generation. To understand underpin stress, one must first re-cast in a positive light their deliberate generation enables achieve critical functions (e.g. synaptic plasticity) through redox signalling (i.e. functionality). Using radicals derivatives signal sensitises when goes awry negative advance mechanistic understanding, we rationalise 13 stress. Key include inter alia unsaturated lipid enrichment, mitochondria, calcium, glutamate, modest antioxidant defence, active transition metals neurotransmitter auto-oxidation. We review RNA oxidation an underappreciated cause complex interplay between each reason dictates susceptibility dynamic context neural identity dependent manner. Our discourse sets stage for investigators interrogate biochemical basis health disease.

Language: Английский

Citations

948

Cardiolipin externalization to the outer mitochondrial membrane acts as an elimination signal for mitophagy in neuronal cells DOI
Charleen T. Chu, Jing Ji, Ruben K. Dagda

et al.

Nature Cell Biology, Journal Year: 2013, Volume and Issue: 15(10), P. 1197 - 1205

Published: Sept. 13, 2013

Language: Английский

Citations

939

Hallmarks of neurodegenerative diseases DOI Creative Commons

David M. Wilson,

Mark Cookson, Ludo Van Den Bosch

et al.

Cell, Journal Year: 2023, Volume and Issue: 186(4), P. 693 - 714

Published: Feb. 1, 2023

Summary

Decades of research have identified genetic factors and biochemical pathways involved in neurodegenerative diseases (NDDs). We present evidence for the following eight hallmarks NDD: pathological protein aggregation, synaptic neuronal network dysfunction, aberrant proteostasis, cytoskeletal abnormalities, altered energy homeostasis, DNA RNA defects, inflammation, cell death. describe hallmarks, their biomarkers, interactions as a framework to study NDDs using holistic approach. The can serve basis defining pathogenic mechanisms, categorizing different based on primary stratifying patients within specific NDD, designing multi-targeted, personalized therapies effectively halt NDDs.

Language: Английский

Citations

801

Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration DOI
Zu‐Hang Sheng, Qian Cai

Nature reviews. Neuroscience, Journal Year: 2012, Volume and Issue: 13(2), P. 77 - 93

Published: Jan. 5, 2012

Language: Английский

Citations

788

Mitochondrial dysfunction and oxidative stress in Parkinson's disease DOI
Sudhakar R. Subramaniam, Marie‐Françoise Chesselet

Progress in Neurobiology, Journal Year: 2013, Volume and Issue: 106-107, P. 17 - 32

Published: April 30, 2013

Language: Английский

Citations

748

Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy DOI
José Á. Obeso, María Stamelou, Christopher G. Goetz

et al.

Movement Disorders, Journal Year: 2017, Volume and Issue: 32(9), P. 1264 - 1310

Published: Sept. 1, 2017

ABSTRACT This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history Dr. James himself what he described accurately missed from today's perspective. disease today is understood as multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology symptomatic treatments, but critically important issues are still pending resolution. Among the latter, need to modify progression undoubtedly priority. In sum, this multiple‐author article, prepared commemorate bicentenary shaking palsy, provides historical state‐of‐the‐art account has been achieved, current situation, how progress toward resolving © 2017 International Parkinson Movement Disorder Society

Language: Английский

Citations

721