The inevitable process of aging affects all tissues of the body and determines the quality and length of life. Human aging is by far the most critical risk factor for the development of several diseases that appear to exclusively affect the elderly, due to mostly unknown reasons (Cummings, 2008; Gladyshev, 2013). While aggressive familial early onset versions of fatal neurodegenerative diseases like Alzheimer’s or Parkinson’s disease can emerge in mid-life, the overwhelming majority of cases develop sporadically in old age, without known genetic causes. Neurons are a prime target for cellular aging. Unlike most other cell types, neurons are mainly born during embryogenesis and then face a demand for life-long performance. Progressive aging also leads to declines in neuronal plasticity and cognitive performances in the majority of healthy people, suggesting that neurons in the brain might decay over their lifetime (Burke and Barnes, 2006; Yankner et al., 2008). Interestingly, transcriptional profiling of different tissues has revealed similar age-related changes across different tissues, including genes involved in stress response, inflammation, and Ca2+ homeostasis, whereas tissue-specific changes of the aging human cortex
