In older individuals with no significant cell loss, a vulnerability of specific cell types to senescence contributes to a decline in cognitive function. As our understanding of molecular and cellular processes for both aging and cognition increase we are likely to find that selective vulnerability can define impairments in particular cognitive domains and will thus define future therapeutic strategies. The effects of age on processes such as oxidative stress, energy metabolism, or DNA damage may differentially influence diverse cell types from excitatory and inhibitory neurons, oligodendrocytes, to cells of the blood brain barrier. Vulnerability of neurons may depend on their size, transmitter system, or location in neural circuits. In other cases, cells may be differentially sensitive due to the function of signaling pathways that underlie homeostasis or mediate cell specific processes involved in cognition (e.g. synaptic plasticity). Systemic influences of inflammation and hormonal status can alter the local milieu to influence different cell populations. Finally, genetic factors related to aging or cognition may define exceptional and pathological aging of specific neural circuits. The current series of articles outline mechanisms for cell selective vulnerability to aging and related these changes to cognitive decline.
In older individuals with no significant cell loss, a vulnerability of specific cell types to senescence contributes to a decline in cognitive function. As our understanding of molecular and cellular processes for both aging and cognition increase we are likely to find that selective vulnerability can define impairments in particular cognitive domains and will thus define future therapeutic strategies. The effects of age on processes such as oxidative stress, energy metabolism, or DNA damage may differentially influence diverse cell types from excitatory and inhibitory neurons, oligodendrocytes, to cells of the blood brain barrier. Vulnerability of neurons may depend on their size, transmitter system, or location in neural circuits. In other cases, cells may be differentially sensitive due to the function of signaling pathways that underlie homeostasis or mediate cell specific processes involved in cognition (e.g. synaptic plasticity). Systemic influences of inflammation and hormonal status can alter the local milieu to influence different cell populations. Finally, genetic factors related to aging or cognition may define exceptional and pathological aging of specific neural circuits. The current series of articles outline mechanisms for cell selective vulnerability to aging and related these changes to cognitive decline.
