No abstract

Dysregulated brain reward systems have been observed in chronic pain. Using functional magnetic resonance imaging (fMRI) and a monetary incentive delay (MID) task, Martucci et al. (2018) showed that neural responses to reward anticipation and outcome are altered in patients with fibromyalgia. The current study aimed to replicate these results in a separate cohort of patients with fibromyalgia recruited at a new location using a similar study design. Twenty patients with fibromyalgia and 20 healthy controls were included in the replication study. Group fMRI analyses revealed a solid and consistent trend of main findings similar to the previous results. Specifically, in the replication cohort of patients with fibromyalgia, medial prefrontal cortex (MPFC) activity was reduced during gain anticipation and increased during no-loss (non-punishment) outcomes, as compared to controls. Similar to the Martucci et al. results, again in the replication cohort, nucleus accumbens activity during gain anticipation did not differ in patients compared to controls. The same behavioral, correlational, and exploratory analyses that were conducted in the Martucci et al. study were conducted in the present replication study, with prior results largely replicated here. Thus, the present replication study results solidify observations of altered cortico-striatal processing to monetary rewards in chronic pain, which underscore relevance of altered brain reward circuits, particularly as related to the MPFC in patients with fibromyalgia.

Cellular senescence is a state of permanent cell cycle arrest that occurs in somatic cells. Cellular senescence is a tightly regulated biological process in normal physiology (Campisi & d'Adda di Fagagna, 2007). However, senescence has also been implicated as a key process in aging, where senescent cells avoid clearance by the immune systems and accumulate to contribute to age-related pathologies (Childs et al., 2015; van Deursen, 2014). In some mouse tissues such as liver, spleen, skin, and lung, it is estimated that the presence of senescence cells increases from ~3%-5% in young tissues to 20%-30% in old tissues (Wang et al., 2009). Indeed, clearance of senescent cells has been demonstrated to delay the onset of aging phenotypes in progeroid mouse models (Baker et al., 2011) and increased metabolic function (Xu et al., 2018) and healthy lifespan (Childs et al., 2015) in naturally aged mice. As targeted removal of senescent cells gains more research interest, there is a need for identifying targets for potential removal of various senescent cell