Mitochondrial function in apoptotic neuronal cell death.
Apoptosis can be defined as the regulated death of a cell and is conducted by conserved pathways. Apoptosis of neurons after injury or disease differs from programed cell death, in the sense that neurons in an adult brain are not "meant" to die and results in a loss of function. Thus apoptosis is an honorable process by a neuron, a cell with limited potential to replace itself, choosing instead to commit suicide to save neighboring cells from release of cellular components that cause injury directly or trigger secondary injury resulting from inflammatory reactions. The excess of apoptosis of neuronal cells underlies the progressive loss of neuronal populations in neurodegenerative disorders and thus is harmful. Mitochondria are the primary source for energy in neurons but are also poised, through the "mitochondrial apoptosis pathway," to signal the demise of cells. This duplicity of mitochondria is discussed, with particular attention given to the specialized case of pathological neuronal cell death.
Haeberlein
Samantha L Budd
SL
Department of Bioscience, AstraZeneca R&D, S-151 85 Södertälje, Sweden. Samantha.budd@astrazeneca.com
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016923:Cell Death; D006801:Humans; D007425:Intracellular Membranes / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D008928:Mitochondria / Q000502:physiology*; D028361:Mitochondrial Diseases / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000166:cytology*; D015398:Signal Transduction / Q000502:physiology