In today's open access paper, researchers present evidence to suggest that the mitochondrial dysfunction that accompanies aging may be a meaningful cause of the loss of neurons that contributes age-related hearing loss, in the sense that it increases the incidence of necroptosis, a form of programmed cell death. Present thinking on the progressive deafness of old age is that the sensory hair cells of the inner ear largely remain intact, but their connection to the brain atrophies - the nerve cells in question dying in excessive numbers for reasons that continue to be explored.

Mitochondria are the power plants of the cell, producing chemical energy store molecules necessary for cellular processes to run, but they are also deeply involved in the various ways in which cells can undergo programmed cell death. With age, mitochondria become less efficient, they become larger the balance between fission and fusion changes, and the quality control mechanism of mitophagy, responsible for removing damaged mitochondria, falters. This contributes to most of the manifestations of aging in some way, and thus it is important for the research community to push ahead in the development of potential means of restoring mitochondrial function in older people.

Mitochondrial Damage and Necroptosis in Aging Cochlea