A well-accepted definition of aging is that it is a time-related progressive loss in the cell capacity to maintain homeostasis. With advancing age, somatic changes come into being because the persistent action of stress conditions is not fully counteracted by cellular repair functions, thus resulting in alterations of organ and system functions. A typical inherent feature of aging is heterogeneity; that is, in addition to genetic individual variability vs. physiological values, vitality is markedly influenced by different lifestyles (Rowe and Kahn, 1987). Thus some elderly individuals age successfully since their aging parameters fall within the adult range; others typically show marked declines of some functions. With specific reference to the brain, the heterogeneity existing among individuals and the different groups of neurons must also be considered when looking for the potential factors and/or the causative events leading to age-related alterations. In this context, it must be stressed that brain aging represents a condition in which pathological changes exist without clinically evident manifestations. At variance with other organs, where the functional and structural units are repeated, the brain is a composite assembly of groups of cells with different metabolic features and functional tasks. Deterioration of function occurs when the number of neurons or their connections decreases below a critical reserve level, and coping with environmental stimulation is seriously hampered. Moreover, the well-documented brain's plastic condition plays a critical role in the balance between deteriorative events and compensating reactions, thus contributing to mask significant changes and to delay decline of function.

In this chapter, we will consider the age-related alterations occurring in the brain on different systems, at cellular and subcellular levels, with the aim to provide a comprehensive view of the many factors and interdependent mechanisms involved in such a multifactorial process.

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