From adolescence to late aging: A comprehensive review of social behavior, alcohol, and neuroinflammation across the lifespan

Impact of High Fat Diet and Ethanol Consumption on Neurocircuitry Regulating Emotional Processing and Metabolic Function

“…The extent of the aforementioned effects of EtOH on neuroimmune responses and neurotoxicity by microglia activity differ depending on length of EtOH exposure, age of exposure, and brain region examined (Chastain and Sarkar, 2014 ; Perkins et al, 2019 ). Studies report microglia are partially activated following binge EtOH exposure which may cause increased production of anti-inflammatory factors (Marshall et al, 2013 ), whereas chronic intermittent EtOH exposure fully activates microglia which increases production of pro-inflammatory cytokines and ROS thereby resulting in neurotoxicity (Qin and Crews, 2012a , b ; Zhao et al, 2013 ).…”

Preface: Setting the stage for understanding alcohol effects in late aging: A special issue including both human and rodent studies

“…Dynamic changes in neuroimmune function across both early development and late aging are the primary topic of the review by Dr. Terrence Deak's research group (Perkins et al, 2020;Chapter 6). Specifically, adolescence appears to be a period of reduced neuroimmune reactivity to most challenges, including alcohol, with lower ambient and substantially impaired induction of neuroimmune genes during this key developmental period (Doremus-Fitzwater et al, 2015).…”

“…A few studies have begun to address this interaction through examination of cytokine and chemokine expression (Gano et al, 2016) as well as microglial density and/or activation state, including several manuscripts included here. The general neuroinflammation response to alcohol is represented symbolically in Figure 1 (black box), which depicts morphological characteristics of microglia as they become more activated (see Perkins et al, 2020 for a more complete elaboration). It would be a mistake, however, to assert that microglial activation state occurs solely as a function of alcohol exposure, or is the sole indicator of alcohol-related neuroinflammation.…”

“…It would be a mistake, however, to assert that microglial activation state occurs solely as a function of alcohol exposure, or is the sole indicator of alcohol-related neuroinflammation. Indeed, despite their role as "primary responders" under conditions of neuroinflammation, morphological changes in microglia tend to be lagging indicators of insult relative to induction of neuroimmune genes (see Perkins et al, 2020 for more detailed discussion). Nevertheless, the intent here is to spur interest in neuroimmune consequences across a more comprehensive range of alcohol consumption/exposure conditions so that the relation between alcohol consumption, neuroinflammation, and neurobehavioral aspects of aging (Figure 1, green box) can be established.…”

“…For instance, late aging in humans suffers a significant transformation in social interaction in which older people tend to interact with fewer social partners, yet their interactions remain deeper and more frequent than younger adults. This narrowing of social circles is thought to reflect a decline in overall social motivational processes which eventually threatens quality of life as bereavement and limited mobility exact their toll later in life (Perkins et al, 2020). The current rises in binge drinking in the elderly are driven by a range of health, social and economic factors that differ as a function of gender (Parikh et al, 2015).…”