title: Role of mitochondrial deterioration in physiological and pathological brain aging.
abstract: BACKGROUND
  Mitochondria are widely reported to occupy a unique role in modulating cell viability, senescence and death. This is consistently supported by the multiple functions of these organelles. In addition to providing the energy for the myriad of cellular performances, mitochondria are involved in regulating thermogenesis, calcium buffering, integration of pro- and anti-apoptotic signals.
  
  
  OBJECTIVE
  To stress the significant importance of subtle, continuous and permanent mitochondrial alterations as key events in physiological aging and as unfavourable determinants of age-related neurodegenerative diseases.
  
  
  RESULTS
  Any dysfunction of these organelles may constitute a serious threat for cellular health status and survival, particularly of post-mitotic nerve and muscle cells. Mitochondrial deterioration may affect discrete features of the organelles (such as their structural dynamics, genetics and physiology) and lead to a progressive functional impairment.
  
  
  CONCLUSIONS
  A variety of mitochondrial tasks, while hampering the possibility to recover the organelles' dysfunctions, offer different and reliable opportunities for therapeutic interventions.
authors.affiliation: Neurobiology of Aging Laboratory, INRCA Research Department, Ancona, Italy. c.bertoni@incra.it
authors.forename: Carlo
authors.initials: C
authors.lastname: Bertoni-Freddari
authors.forename: Patrizia
authors.initials: P
authors.lastname: Fattoretti
authors.forename: Belinda
authors.initials: B
authors.lastname: Giorgetti
authors.forename: Moreno
authors.initials: M
authors.lastname: Solazzi
authors.forename: Marta
authors.initials: M
authors.lastname: Balietti
authors.forename: William
authors.initials: W
authors.lastname: Meier-Ruge
mesh_terms: D000375:Aging; D001921:Brain / Q000648:ultrastructure*; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000648:ultrastructure*; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000473:pathology* / Q000628:therapy