In Drosophila, neuropeptide Pigment Dispersing Factor (PDF) is expressed in small and large ventral Lateral Neurons (sLNv and lLNv), among which sLNv are critical for activity rhythms in constant darkness. Studies show that this is mediated by rhythmic accumulation and likely secretion of PDF from sLNv dorsal projections, which in turn synchronises molecular oscillations in downstream circadian neurons. Using targeted expression of a neurodegenerative protein Huntingtin in LNv, we evoke a selective loss of neuropeptide PDF and clock protein PERIOD from sLNv soma. However, PDF is not lost from sLNv dorsal projections and lLNv. These flies are behaviourally arrhythmic in constant darkness despite persistence of PDF oscillations in sLNv dorsal projections and synchronous PERIOD oscillations in downstream circadian neurons. We find that PDF oscillations in sLNv dorsal projections are not sufficient for sustenance of activity rhythms in constant darkness and this is suggestive of an additional component that is possibly dependent on sLNv molecular clock and PDF in sLNv soma. Additionally, despite loss of PERIOD in sLNv, their activity rhythms entrain to light/dark cycles indicating that sLNv molecular clocks are not necessary for entrainment. Under constant light, these flies lack PDF from both soma and dorsal projections of sLNv, and when subjected to light/dark cycles, show morning and evening anticipation and accurately phased morning and evening peaks. Thus, under light/dark cycles, PDF in sLNv is not necessary for morning anticipation.

Alzheimer’s disease (AD) is the most common cause of dementia. The APOE -ε4 allele of the apolipoprotein E ( APOE ) gene is the strongest genetic risk factor for late-onset AD. The APOE genotype modulates the effect of sleep disruption on AD risk, suggesting a possible link between apoE and sleep in AD pathogenesis, which is relatively unexplored. We hypothesized that apoE modifies Aβ deposition and Aβ plaque–associated tau seeding and spreading in the form of neuritic plaque–tau (NP-tau) pathology in response to chronic sleep deprivation (SD) in an apoE isoform–dependent fashion. To test this hypothesis, we used APPPS1 mice expressing human APOE -ε3 or -ε4 with or without AD-tau injection. We found that SD in APPPS1 mice significantly increased Aβ deposition and peri-plaque NP-tau pathology in the presence of APOE4 but not APOE3. SD in APPPS1 mice significantly decreased microglial clustering around plaques and aquaporin-4 ( AQP4 ) polarization around blood vessels in the presence of APOE4 but not APOE3. We also found that sleep-deprived APPPS1:E4 mice injected with AD-tau had significantly altered sleep behaviors compared with APPPS1:E3 mice. These findings suggest that the APOE -ε4 genotype is a critical modifier in the development of AD pathology in response to SD.

Increased attention to the prevalence and impact of traumatic experiences have been highlighted within the mental health field since Felitti et al.'s study of adverse childhood experiences. Black communities experience traumatic events at a higher rate than other racial groups. The phenomena of historical trauma, race-based trauma, and intergenerational trauma have been speculated to be reasons for this discrepancy. In this article, the authors explore factors that compound the traumatic experiences of Black communities, review socioculturally attuned family therapy and trauma-informed care, and propose an approach to addressing intergenerational trauma in Black families that integrates socioculturally attuned family therapy and trauma-informed care.

Counseling theories created by White theorists have traditionally failed to consider the religious or spiritual experiences of Black clients. Integration of Black liberation theology and narrative therapy provides a novel approach to support counseling trainees in meeting the needs of Black clients. Decolonizing therapeutic strategies are presented along with counselor educator recommendations.