‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease

By C. S. Chan, Jaime N. Guzmán, E. Ilijic, Jeff N. Mercer, C. Rick, T. Tkatch, G. Meredith, D. Surmeier. Nature, 2007

903 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/fa5b2ffae92a946198c65f0c31b5de922a7af111

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Neuronal voltage-gated calcium channels: structure, function, and dysfunction. (2014, background): “3 channels regulate the pacemaking of dopaminergic neurons in the substantia nigra in an age-dependent manner, with older neurons increasingly relying on this channel type (Chan et al., 2007).”
PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (2010, background): “, mammalian tissues may contain pathways orthologous to those recently identified in yeast [54,55]); the ability of the tissue to mitigate the damage by other means (a tissue composed of mitotic cells may be able to manage mitochondrial damage through cellular turnover rather than mitochondrial turn”
Intrinsic Membrane Hyperexcitability of ALS Patient-Derived Motor Neurons (2014, background): “Calcium overload through voltage-gated calcium channels (Chan et al., 2007) and activation of ER stress (Saxena and Caroni, 2011) are possibilities.”
Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “Further, similar to calbindin, Ca2+ channel antagonists dimin‐ ish the sensitivity of SNc dopamine neurons to mitochondrial toxins (Chan et al., 2007).”
PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death (2009, neutral): “634 Molecular Cell 33, 627–638, March 13, 2009 ª2009 Elsevier Inc. mitochondria (Chan et al., 2007).”
The energy cost of action potential propagation in dopamine neurons: clues to susceptibility in Parkinson's disease (2013, methodology): “…dysfunction, inability to deal with protein turnover and impaired autophagy, all factors that are considered to contribute to cell death in PD (Chan et al., 2007; Sulzer, 2007; Schapira, 2008; Gasser, 2010; Guzman et al., 2010; Martin et al., 2010; Obeso et al., 2010; Surmeier et al.,…”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “Adult ventrolateral SNc DA neurons engage L-type Ca v 1.3 calcium channels for rhythmic pacemaking, in contrast to less vulnerable DA neurons of the ventral tegmental area which use sodium channels for pake-macing activity (Chan et al , 2007).”
The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (2015, background): “3 are expressed andboth isoformsare often even expressed in the same cell, such as in neurons (Olson et al., 2005; Chan et al., 2007; Dragicevic et al., 2014), adrenal chromaffin cells (Marcantoni et al., 2010), and sinoatrial node (SAN) and atrial cardiomyocytes (Mangoni et al., 2003).”