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Abstract Background There is an urgent need to measure the psychological toll of climate-related ecological degradation and destruction in low- and middle-income countries. However, availability of locally adapted tools is limited. Our objective was to conduct a transcultural translation and cultural adaptation (TTA) of the Solastalgia subscale of the Environmental Distress Scale (EDS-Solastalgia) in Kilifi, Kenya, which is undergoing transformational changes due to climate change. Methods We conducted 5 expert interviews, 2 Focus Group Discussions (n = 22) and 10 cognitive interviews to solicit feedback on the EDS along the following cultural equivalency domains: Comprehensibility (Semantic equivalence); Relevance (Content equivalence); Response set (Technical equivalence) and Completeness (Semantic, criterion and conceptual equivalence). Results After an initial translation and back translation of the EDS-Solastalgia, respondents identified several terms that needed to be altered to make the scale understandable, less technical and culturally acceptable. For some items, respondents recommended examples to be included to aid comprehensibility. Feedback from respondents were iteratively integrated into the Swahili EDS-Solastalgia scale, and final endorsement of all changes were confirmed during cognitive interviews. Discussion The culturally adapted Swahili EDS-Solastalgia scale needs to be tested for its psychometric properties prior to utilization in survey studies to quantitatively establish the burden of climate-related distress and test for associations with common mental health conditions.

The present chapter summarizes the clinical and preclinical findings collected to date, showing the impact of developmental alcohol exposure on sleep physiology. Sleep is a complex physiological process that plays a pivotal role in maintaining overall health and well-being via its involvement in regulating physiological, cognitive, and emotional functions. Clinical studies consistently report a high prevalence of sleep disturbances in children and adolescents diagnosed with fetal alcohol spectrum disorders (FASDs), including short sleep duration, sleep anxiety, bedtime resistance, increased sleep fragmentation, and parasomnias. It is established that alcohol consumption during gestation impairs brain development, leading to structural and functional alterations that may affect sleep architecture. In addition, clinical investigations have found a significant correlation between sleep-wake cycle disruptions and cognitive impairments after developmental alcohol exposure, and sleep disturbances are increasingly recognized as a substantial problem among FASD patients. However, the molecular mechanisms underlying these disturbances are poorly understood. Surprisingly, few studies with animal models of FASDs have characterized the effect of developmental ethanol exposure on sleep physiology, and these have focused on high doses. This chapter provides an overview of the current knowledge, reports the sleep disturbances in FASD patients, and then summarizes the gap in understanding the molecular and physiological mechanisms.

Adolescence is a conserved neurodevelopmental period encompassing maturation of glia and the innate immune system that parallels refinement of brain structures, neurotransmitter systems, and neurocircuitry. Given the vast neurodevelopmental processes occurring during adolescence, spanning brain structural and neurocircuitry refinement to maturation of neurotransmitter systems, glia, and the innate immune system, insults incurred during this critical period of neurodevelopment, could have profound effects on brain function and behavior that persist into adulthood. Adolescent binge drinking is common and associated with many adverse outcomes that may underlie the lifelong increased risk of alcohol-related problems and development of an alcohol use disorder (AUD). In this chapter, we examined the impact of adolescent binge drinking models using the adolescent intermittent ethanol (AIE) model on adult neurobiology. These studies implicate proinflammatory neuroimmune signaling across glia and neurons in persistent AIE-induced neuropathology. Some of these changes are reversible, providing unique opportunities for the development of treatments to prevent many of the long-term consequences of adolescent alcohol misuse.

Alcohol use disorder (AUD) is a highly prevalent, complex, multifactorial and heterogeneous disorder, with 11 % and 30 % of adults meeting criteria for past-year and lifetime AUD, respectively. Identification of the molecular mechanisms underlying risk for AUD would facilitate effective deployment of personalized interventions. Studies using rhesus monkeys and rats, have demonstrated that individuals with low cognitive flexibility and a predisposition towards habitual behaviors show an increased risk for future heavy drinking. Further, low cognitive flexibility is associated with reduced dorsolateral prefrontal cortex (dlPFC) function in rhesus monkeys. To explore the underlying unique molecular signatures that increase risk for chronic heavy drinking, a genome-wide DNA methylation (DNAm) analysis of the alcohol-naïve dlPFC-A46 biopsy prior to chronic alcohol self-administration was conducted. The DNAm profile provides a molecular snapshot of the alcohol-naïve dlPFC, with mapped genes and associated signaling pathways that vary across individuals. The analysis identified 1,463 differentially methylated regions (DMRs) related to unique genes that were strongly associated with average ethanol intake consumed over 6 months of voluntary self-administration. These findings translate behavioral phenotypes into neural markers of risk for AUD, and hold promise for parallel discoveries in risk for other disorders involving impaired cognitive flexibility. SIGNIFICANCE: Alcohol use disorder (AUD) is a highly prevalent and heterogeneous disorder. Prevention strategies to accurately identify individuals with a high risk for AUD, would help reduce the prevalence, and severity of AUD. Our novel epigenomic analysis of the alcohol-naïve nonhuman primate cortex provides a molecular snapshot of the vulnerable brain, pointing to circuitry and molecular mechanisms associated with cortical development, synaptic functions, glutamatergic signaling and coordinated signaling pathways. With a complex disorder like AUD, having the ability to identify the molecular mechanisms underlying AUD risk is critical for better development of personalized effective treatments.

The Eastern Mediterranean and Middle East region, where both natural and anthropogenic disasters have occurred, is particularly vulnerable to the effects of climate change. This article aims to alert and inform the neurological community about the many health risks linked to climate change, including some more specific ones, such as the mucilage phenomenon, heat waves and dust storms, and the spread of vector-borne infections. We describe the potential adverse effects of such climate-related exposures and advocate for more research to promote Brain Health.

Understanding factors that alter the effect of alcohol in biological systems has been an area of active investigation for several decades. Recently, it has become clear that age is one of the most salient factors influencing how both acute and chronic alcohol exposure alters behavioral function. The following book chapter discusses how alcohol produces differential effects in adolescent animals in comparison to adult and aged (i.e., older) animals. Furthermore, where possible, relevant research identifying possible brain mechanisms mediating the differential effects of alcohol will be discussed. Finally, we highlight a small number of studies where sex and age of the subject interact to modify cognitive impairments produced by alcohol. We conclude that much work still needs to be done to fully understand how age, sex, and alcohol interact to produce the wide range of effects caused by consumption of the drug.

Abstract To investigate the effects of moderate ethanol exposure on glucose metabolism in APP/PS1 mice, an early-onset Alzheimer’s disease (AD) mouse model, we employed an fluoro-deoxy-glucose (FDG)-micro-positron emission tomography (PET). We also utilized the comprehensive lab animal monitoring system (CLAMS) to measure whole-body energy expenditure and respiratory exchange ratio (RER). We found that ethanol exposure increased glucose metabolism in the brain as measured by FDG-PET. Also, CLAMS data indicated a decrease in RER, suggesting a shift toward fat utilization as the primary energy source. Following ethanol exposure in APP/PS1 mice, these findings reveal a distinct metabolic difference between brain and peripheral tissues.

ABSTRACTRenewed scientific interest in sympathetic modulation of muscle and neuromuscular junctions has spurred a flurry of new discoveries with major implications for motor diseases. However, the role sympathetic axons play in the persistent dysfunction that occurs after nerve injuries remains to be explored. Peripheral nerve injuries are common and lead to motor, sensory, and autonomic deficits that result in lifelong disabilities. Given the importance of sympathetic signaling in muscle metabolic health and maintaining bodily homeostasis, it is imperative to understand the regenerative capacity of sympathetic axons after injury. Therefore, we tested sympathetic axon regeneration and functional reinnervation of skin and muscle, both acute and long-term, using a battery of anatomical, pharmacological, chemogenetic, cell culture, analytical chemistry, and electrophysiological techniques. We employed several established growth-enhancing interventions, including electrical stimulation and conditioning lesion, as well as an innovative tool called bioluminescent optogenetics. Our results indicate that sympathetic regeneration is not enhanced by any of these treatments and may even be detrimental to sympathetic regeneration. Despite the complete return of motor reinnervation after sciatic nerve injury, gastrocnemius muscle atrophy and deficits in muscle cellular energy charge, as measured by relative ATP, ADP, and AMP concentrations, persisted long after injury, even with electrical stimulation. We suggest that these long-term deficits in muscle energy charge and atrophy are related to the deficiency in sympathetic axon regeneration. New studies are needed to better understand the mechanisms underlying sympathetic regeneration to develop therapeutics that can enhance the regeneration of all axon types.

Alcohol and cannabis are often taken in combination, and extensive co-use has been linked to enduring changes in cognitive and metabolic functioning. The underlying mechanisms for these effects are unclear, but we recently demonstrated that co-administration of ethanol and delta-9-tetrahydrocannbinol (THC) to adolescent rats caused lasting adaptations in GABA and glycogen synthase kinase 3ß (GSK3ß) signaling in the medial prefrontal cortex (mPFC). As a ubiquitous protein kinase, GSK3ß is downstream to the protein kinase B (also known as AKT) pathway that is activated by insulin receptor signaling in a main control center for metabolism and energy homeostasis, the mediobasal hypothalamus (MBH). Our goal here was to investigate if volitional co-use of low to moderate levels of ethanol and THC would impact the total and phosphorylated levels (p) of AKT and GSK3ß in the mPFC and MBH. Peri-adolescent Long Evans rats [postnatal day (P) 30-47] consumed 10 % ethanol, cookies laced with THC (3-10 mg/kg/day), both drugs, or vehicle controls. On P114, we modeled re-exposure to a behaviorally relevant dose of THC by challenging rats (i.p.) with 5 mg/kg THC (or vehicle) and sacrificed them 30 min later. Western blot analysis revealed that THC challenge increased pAKT and pGSK3ß compared to control similarly across all treatment groups, sexes, and brain regions; no effects on total levels of AKT or GSK3ß were found. Previously reported behavioral results from these rats showed no differences in working memory assessed in adulthood. Although future studies will be necessary to determine the role of exposure dose on drug-induced adaptations in AKT and GSK3ß signaling, the current findings suggest that moderate volitional co-use of alcohol and THC may not produce long-term deficits that persist into adulthood.