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

Cold Spring Harbor Perspectives in Biology, Год журнала: 2015, Номер 7(6), С. a020628 - a020628

Опубликована: Апрель 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

Язык: Английский

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

Cell, Год журнала: 2012, Номер 148(6), С. 1145 - 1159

Опубликована: Март 1, 2012

Язык: Английский

Процитировано

2943

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

Molecular Cell, Год журнала: 2012, Номер 48(2), С. 158 - 167

Опубликована: Окт. 1, 2012

Язык: Английский

Процитировано

2349

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

Nature, Год журнала: 2014, Номер 505(7483), С. 335 - 343

Опубликована: Янв. 14, 2014

Язык: Английский

Процитировано

1587

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

и другие.

Cell, Год журнала: 2011, Номер 147(4), С. 893 - 906

Опубликована: Ноя. 1, 2011

Язык: Английский

Процитировано

1105

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

Maria Luisa Fiorello,

Damian M. Bailey

и другие.

Redox Biology, Год журнала: 2018, Номер 15, С. 490 - 503

Опубликована: Фев. 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.

Язык: Английский

Процитировано

956

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

и другие.

Nature Cell Biology, Год журнала: 2013, Номер 15(10), С. 1197 - 1205

Опубликована: Сен. 13, 2013

Язык: Английский

Процитировано

943

Hallmarks of neurodegenerative diseases DOI Creative Commons

David M. Wilson,

Mark Cookson, Ludo Van Den Bosch

и другие.

Cell, Год журнала: 2023, Номер 186(4), С. 693 - 714

Опубликована: Фев. 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.

Язык: Английский

Процитировано

846

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

Nature reviews. Neuroscience, Год журнала: 2012, Номер 13(2), С. 77 - 93

Опубликована: Янв. 5, 2012

Язык: Английский

Процитировано

789

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

Progress in Neurobiology, Год журнала: 2013, Номер 106-107, С. 17 - 32

Опубликована: Апрель 30, 2013

Язык: Английский

Процитировано

751

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

и другие.

Movement Disorders, Год журнала: 2017, Номер 32(9), С. 1264 - 1310

Опубликована: Сен. 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

Язык: Английский

Процитировано

723