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Aging with alcohol-related brain damage: Critical brain circuits associated with cognitive dysfunction
Polliana Toledo Nunes1, Brian T Kipp1, Nicole L Reitz1
1Developmental Exposure Alcohol Research Center, Behavioral Neuroscience Program, Department of Psychology, Binghamton University, State University of New York, Binghamton, NY, United States.
International Review of Neurobiology
|November 18, 2019
Summary
Alcoholism and thiamine deficiency harm the brain, with age significantly impacting outcomes. Adolescent alcohol exposure shows lasting effects, highlighting the need to study alcohol
Area of Science:
- Neuroscience
- Toxicology
- Gerontology
Background:
- Alcoholism causes brain damage and cognitive deficits, influenced by alcohol, thiamine deficiency, and age.
- The interplay of these factors in alcohol-related brain damage (ARBD) remains unclear.
- Age at exposure and aging with ARBD are critical but understudied variables.
Purpose of the Study:
- To investigate the distinct and combined effects of ethanol toxicity and thiamine deficiency on neuroinflammation, neuronal loss, and cognitive function.
- To examine the influence of age at exposure (adolescence vs. adulthood) and subsequent aging on ARBD.
- To understand how different drinking patterns and thiamine deficiency impact brain aging and cognitive trajectories.
Main Methods:
- Utilized pre-clinical models to assess neuroinflammation, neuronal phenotypes, neurogenesis, and behavioral impairments.
- Administered acute thiamine deficiency, chronic adult ethanol exposure, and adolescent intermittent ethanol exposure.
- Evaluated effects across different brain regions (thalamus, hippocampus, frontal cortex, basal forebrain) and assessed behavioral outcomes.
Main Results:
- Thiamine deficiency caused significant neuroinflammation and thalamic lesions; chronic adult ethanol had minimal neuroinflammatory effects.
- Adolescent intermittent ethanol exposure induced persistent neuroinflammation in the hippocampus and frontal cortex.
- All conditions led to cholinergic deficits, reduced hippocampal neurogenesis, and frontal cortex alterations, with thiamine deficiency causing the most severe behavioral impairments.
Conclusions:
- Thiamine deficiency and adolescent intermittent ethanol exposure have distinct and lasting impacts on brain structure and function.
- Age and aging processes significantly modulate the neuropathology and cognitive consequences of alcohol exposure.
- Further research is needed to understand how alcohol consumption across the lifespan affects brain aging and disease progression.
Keywords:
AgingAlcoholBasal forebrainCognitionDevelopmentEtOHFrontal cortexHippocampusHumanMemoryMouseNeuroinflammationRatThalamusMore Related Videos
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