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Determinants of dopaminergic neuron loss in Parkinson's disease

The FEBS journal, 2018-10, Vol.285 (19), p.3657-3668 [Peer Reviewed Journal]

2018 Federation of European Biochemical Societies ;2018 Federation of European Biochemical Societies. ;Copyright © 2018 Federation of European Biochemical Societies ;ISSN: 1742-464X ;EISSN: 1742-4658 ;DOI: 10.1111/febs.14607 ;PMID: 30028088

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  • Title:
    Determinants of dopaminergic neuron loss in Parkinson's disease
  • Author: Surmeier, Dalton James
  • Subjects: autophagy ; axon ; bioenergetics ; calcium ; dopamin ; Dopamine receptors ; Ecstasy ; lewy pathology ; Mitochondria ; Movement disorders ; Neurodegenerative diseases ; Neurons ; Parkinson's disease ; Parkinsons disease ; Pathogenesis ; Pathology ; Phenotypes ; Substantia nigra ; Synuclein
  • Is Part Of: The FEBS journal, 2018-10, Vol.285 (19), p.3657-3668
  • Description: The cardinal motor symptoms of Parkinson's disease (PD) are caused by the death of dopaminergic neurons in the substantia nigra pars compacta (SNc). Alpha‐synuclein (aSYN) pathology and mitochondrial dysfunction have been implicated in PD pathogenesis, but until recently it was unclear why SNc dopaminergic neurons should be particularly vulnerable to these two types of insult. In this brief review, the evidence that SNc dopaminergic neurons have an anatomical, physiological, and biochemical phenotype that predisposes them to mitochondrial dysfunction and synuclein pathology is summarized. The recognition that certain traits may predispose neurons to PD‐linked pathology creates translational opportunities for slowing or stopping disease progression. This review summarizes evidence that selective neuronal vulnerability in Parkinson's disease results from several phenotypic traits: (a) calcium‐dependent, feed‐forward control of mitochondrial respiration leading to elevated reactive oxygen species and cytosolic calcium concentration; (b) an extensive axonal arbor; and (c) a reactive neurotransmitter. These traits increase vulnerability to genetic mutations associated with PD, age and environmental toxins.
  • Publisher: England: Blackwell Publishing Ltd
  • Language: English
  • Identifier: ISSN: 1742-464X
    EISSN: 1742-4658
    DOI: 10.1111/febs.14607
    PMID: 30028088
  • Source: Geneva Foundation Free Medical Journals at publisher websites
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