As organisms age, circadian rhythms tend to dampen as demonstrated in behavioral and molecular experiments both in mammals (Reddy and O'Neill, 2010) and Drosophila (Giebultowicz and Long, 2015). This phenomenon is implicated in declining cellular homeostasis and in various pathologies of aging, including altered inflammatory responses (Fonken et al., 2016), neurodegenerative diseases (Musiek et al., 2013) and impaired memory formation (Kondratova et al., 2010). In addition, physiological aging and late life diseases are accelerated by chronic disruption of clock functions in mammals (Kondratov et al., 2006; Antoch et al., 2008; Yu and Weaver, 2011; Hastings and Goedert, 2013). Similar to mammals, mutations in core clock genes accelerate aging phenotypes in Drosophila (Krishnan et al., 2009). Disruptions of the circadian clock in flies predispose them to neurodegeneration, although it is not known which clocks are involved (Krishnan et al., 2009, 2012). It was shown that Drosophila per01 mutants have increased levels of oxidative damage and neurodegeneration compared to age-matched controls (Krishnan et al., 2009). However, it is not known to what extent per mRNA is expressed in the glia, and consequently, whether loss of per in these cells could contribute to neurodegeneration and aging in general.