Abstract
Excessive alcohol consumption results in neurodegeneration which some hypothesize is caused by neuroinflammation. One characteristic of neuroinflammation is microglial activation, but it is now well accepted that microglial activation may be pro- or anti-inflammatory. Recent work indicates that the Majchrowicz model of alcohol-induced neurodegeneration results in anti-inflammatory microglia, while intermittent exposure models with lower doses and blood alcohol levels produce microglia with a pro-inflammatory phenotype. To determine the effect of a repeated binge alcohol exposure, rats received two cycles of the four-day Majchrowicz model. One hemisphere was then used to assess microglia via immunohistochemistry and while the other was used for ELISAs of cytokines and growth factors. A single binge ethanol exposure resulted in low-level of microglial activation; however, a second binge potentiated the microglial response. Specifically, double binge rats had greater OX-42 immunoreactivity, increased ionized calcium-binding adapter molecule 1 (Iba-1+) cells, and upregulated tumor necrosis factor-α (TNF-α) compared with the single binge ethanol group. These data indicate that prior ethanol exposure potentiates a subsequent microglia response, which suggests that the initial exposure to alcohol primes microglia. In summary, repeated ethanol exposure, independent of other immune modulatory events, potentiates microglial activity.
Highlights
14% of the United States population meets the diagnostic criteria for an alcohol use disorder (AUD) in any given year [1]
Understanding the mechanisms that underlie or contribute to alcohol-induced neurodegeneration may provide a novel therapeutic target to ameliorate damage and prevent the downward spiral into an AUD [14,84]. These studies present a novel view of the impact of alcohol abuse on microglial activity
Data presented indicate that alcohol causes a shift in microglial phenotypes to a primed state
Summary
14% of the United States population meets the diagnostic criteria for an alcohol use disorder (AUD) in any given year [1]. Due to its preventable nature, alcoholism traditionally has not been defined as a neurodegenerative disorder, but chronic, excessive consumption may cause damage in the temporal lobe on par with diseases such as Alzheimer’s [4]. Alcoholic-related dementia is the second leading cause of dementia in the United States only behind Alzheimer’s disease [9,10]. Alcohol-induced neurodegeneration and the associated cognitive deficits are thought to be critical factors in the development of AUDs [13,14,15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
