Parthanatos: PARP- and AIF-dependent programmed cell death

Research output: Chapter in Book/Report/Conference proceedingChapter


In the nervous system, cell death is important during development, replacement of mitotic cells, and for remodeling. Cell death in response to traumatic, ischemic, or intrinsic events can lead to loss of normal function in diseases of the nervous system ranging from traumatic brain injury, stroke, neurodegenerative diseases, demyelinating diseases, and cancer. The pathways toward cell death in the nervous system have been of scientific and medical interest. During development, there is programmed cell death that follows criteria originally described by Lockshin and colleagues in insect cells (1) and subsequently extend into understanding the development of the mammalian nervous system. Outside of development, it is not clear if programmed cell death continues to play a role. Apoptosis and necrosis were originally defined morphologically (2), and subsequently, biochemical pathways for apoptosis have been intensively studied and defined. Activation of caspases is the defining biochemical feature of apoptosis. Apoptosis can occur in the nervous system in restricted settings, but in most cases, cell death does not conform to the morphologic criteria of apoptosis and is caspase independent. Autophagy, originally defined as a mechanism to recycle organelles and proteins, has emerged as a potentially important response to diseases involving misfolded proteins and thus may be important in certain neurodegenerative diseases. Interference with the autophagic process can lead to neurodegenerative phenotypes in mice (3-5).

Original languageEnglish (US)
Title of host publicationBeyond Apoptosis
Subtitle of host publicationCellular Outcomes of Cancer Therapy
PublisherCRC Press
Number of pages14
ISBN (Electronic)9781420020502
ISBN (Print)084939192X, 9780849391927
StatePublished - Jan 1 2008

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)


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