% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Exner:136580,
      author       = {Exner, Nicole and Müller-Rischart, Anne Kathrin and Haass,
                      Christian and Winklhofer, Konstanze F},
      title        = {{M}itochondrial dysfunction in {P}arkinson's disease:
                      molecular mechanisms and pathophysiological consequences.},
      journal      = {The EMBO journal},
      volume       = {31},
      number       = {14},
      issn         = {0261-4189},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2020-02902},
      pages        = {3038-3062},
      year         = {2012},
      abstract     = {Neurons are critically dependent on mitochondrial integrity
                      based on specific morphological, biochemical, and
                      physiological features. They are characterized by high rates
                      of metabolic activity and need to respond promptly to
                      activity-dependent fluctuations in bioenergetic demand. The
                      dimensions and polarity of neurons require efficient
                      transport of mitochondria to hot spots of energy
                      consumption, such as presynaptic and postsynaptic sites.
                      Moreover, the postmitotic state of neurons in combination
                      with their exposure to intrinsic and extrinsic neuronal
                      stress factors call for a high fidelity of mitochondrial
                      quality control systems. Consequently, it is not surprising
                      that mitochondrial alterations can promote neuronal
                      dysfunction and degeneration. In particular, mitochondrial
                      dysfunction has long been implicated in the etiopathogenesis
                      of Parkinson's disease (PD), based on the observation that
                      mitochondrial toxins can cause parkinsonism in humans and
                      animal models. Substantial progress towards understanding
                      the role of mitochondria in the disease process has been
                      made by the identification and characterization of genes
                      causing familial variants of PD. Studies on the function and
                      dysfunction of these genes revealed that various aspects of
                      mitochondrial biology appear to be affected in PD,
                      comprising mitochondrial biogenesis, bioenergetics,
                      dynamics, transport, and quality control.},
      subtyp        = {Review Article},
      keywords     = {Animals / Humans / Mitochondria: genetics / Mitochondria:
                      metabolism / Mitochondria: pathology / Neurons: metabolism /
                      Neurons: pathology / Parkinson Disease: genetics / Parkinson
                      Disease: metabolism / Parkinson Disease: pathology},
      cin          = {AG Winklhofer / AG Haass},
      ddc          = {570},
      cid          = {I:(DE-2719)5000047 / I:(DE-2719)1110007},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:22735187},
      pmc          = {pmc:PMC3400019},
      doi          = {10.1038/emboj.2012.170},
      url          = {https://pub.dzne.de/record/136580},
}