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Human Alcohol-Related Neuropathology

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Human Alcohol-Related Neuropathology Acta Neuropathol (2014) 127:71–90 DOI 10.1007/s00401-013-1233-3 REVIEW Human alcohol-related neuropathology Suzanne M. de la Monte · Jillian J. Kril Received: 15 October 2013 / Revised: 12 December 2013 / Accepted: 13 December 2013 / Published online: 27 December 2013 © Springer-Verlag Berlin Heidelberg 2013 Abstract Alcohol-related diseases of the nervous sys- on glia, myelin, and the microvasculature. Alcohol also tem are caused by excessive exposures to alcohol, with has devastating neurotoxic and teratogenic effects on the or without co-existing nutritional or vitamin deficiencies. developing brain in association with fetal alcohol spectrum Toxic and metabolic effects of alcohol (ethanol) vary with disorder/fetal alcohol syndrome. Alcohol impairs function brain region, age/developmental stage, dose, and duration of neurons and glia, disrupting a broad array of functions of exposures. In the mature brain, heavy chronic or binge including neuronal survival, cell migration, and glial cell alcohol exposures can cause severe debilitating diseases (astrocytes and oligodendrocytes) differentiation. Further of the central and peripheral nervous systems, and skele- progress is needed to better understand the pathophysiol- tal muscle. Most commonly, long-standing heavy alcohol ogy of this exposure-related constellation of nervous sys- abuse leads to disproportionate loss of cerebral white mat- tem diseases and better correlate the underlying pathology ter and impairments in executive function. The cerebellum with in vivo imaging and biochemical lesions. (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degenera- Overview: alcohol use guidelines, abuse, metabolism tion. Although all cell types within the nervous system are and toxicity, public health problems and established vulnerable to the toxic, metabolic, and degenerative effects limits of alcohol, astrocytes, oligodendrocytes, and synaptic ter- minals are major targets, accounting for the white matter After tobacco and obesity, alcohol abuse is the third lead- atrophy, neural inflammation and toxicity, and impairments ing preventable cause of death in the United States. Fur- in synaptogenesis. Besides chronic degenerative neuro- thermore, the alcohol abuse death rate is nearly doubled pathology, alcoholics are predisposed to develop severe by including the premature deaths that are alcohol-related, potentially life-threatening acute or subacute symmetrical e.g., motor vehicle accidents. Heavy drinking wors- hemorrhagic injury in the diencephalon and brainstem due ens morbidity from chronic disease as it exacerbates the to thiamine deficiency, which exerts toxic/metabolic effects effects of hypertension, diabetes mellitus, and hepatitis, and interferes with the metabolism and therapeutic actions of various medications. Societal costs of alcohol abuse S. M. de la Monte (*) are extremely high due to increased rates of severe injury, Departments of Pathology (Neuropathology), Neurology, accidental deaths, lost income, over use of healthcare and Medicine, Rhode Island Hospital and the Warren Alpert resources, and disruption of the family life [17]. Since dis- Medical School of Brown University, 55 Claverick Street, Room 419, Providence, RI 02903, USA ease-related effects of alcohol can occur with either chronic e-mail: [email protected] or binge drinking, the National Institutes of Alcohol Abuse and Alcoholism (NIAAA) established guidelines for (non- J. J. Kril disease risk) acceptable upper limits of alcohol intake by Disciplines of Medicine and Pathology, Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia adults. For men aged 21–65 years, the NIAAA recom- e-mail: [email protected] mends a maximum of 14 standard drinks per week and four 1 3 72 Acta Neuropathol (2014) 127:71–90 drinks on any given day, whereas for women in the same where it is degraded to acetaldehyde followed by acetate, age bracket, and men over 65, the recommended upper lim- and then CO H O. There are three major pathways of 2 + 2 its are seven standard drinks per week and three drinks on alcohol metabolism: (1) alcohol dehydrogenase–aldehyde any given day. dehydrogenase; (2) microsomal ethanol oxidizing sys- Standard drinks all contain the same quantity of alcohol, tem (MEOS); and (3) catalase. With low levels of alcohol, although the definition of a standard drink and the recom- aldehyde dehydrogenase is the principal enzyme utilized mended upper limits of alcohol intake vary by country. In for metabolism. With high levels of alcohol, MEOS is the USA, one standard drink equals 14 grams of pure alco- recruited into action. The same enzymatic pathways exist in hol which is contained in 12 oz (355 ml) of beer or cooler the brain. However, in the liver, different isoforms of alco- (5 % alcohol), 5 oz (148 ml) of wine (12 % alcohol), 1.5 oz hol and acetaldehyde dehydrogenases may be preferentially (44 ml) of 80-proof spirits (40 % alcohol), 8 oz (237 ml) of utilized. However, more research is needed to understand malt liquor (7 % alcohol), or 3 oz (89 ml) of fortified wine the consequences and limitations of the brain’s differential (http://www.niaaa.nih.gov/alcohol-health/overview-alco- use of selected alcohol-metabolizing enzyme pathways. hol-consumption/standard-drink). In Australia and New Zealand, a standard drink is 10 g ethanol and upper limits of 4 drinks per day and 14 per week are recommended (htt Alcohol-induced brain injury: indirect effects p://www.drinkwise.org.au/you-alcohol/alcohol-facts/what- is-a-standard-drink/). In Japan, a standard drink contains Growing evidence suggests that alcohol-mediated brain 19.75 g alcohol, whereas in the United Kingdom, a stand- injury may be partly consequential to liver injury via a ard drink has 8 g alcohol. In the European Union, the alco- liver–brain axis [34]. Therefore, it is highly relevant that hol content in a standard drink varies by country, ranging neuropathologists and neuroscientists understand the struc- from 6 to 17 g (http://www.icap.org/PolicyIssues/Drinking tural and functional effects of alcohol on the liver. Alcohol- Guidelines/StandardDrinks/KeyFactsandIssues/tabid/209/ mediated injury compromises the liver’s capacity to detox- Default.aspx). Most guidelines recommend abstinence for ify ethanol and thereby protect the brain and other organs pregnant women or those breastfeeding, and reduced intake from the toxic effects of ethanol and acetaldehyde. In in the elderly or persons on medications. addition, chronic liver injury leads to production of toxic, metabolic, and inflammatory mediators that injure the Alcohol abuse brain [28, 34]. In brief, alcohol-induced liver injury can be divided into 3 stages. Stage 1 is fatty liver disease (hepatic The rates of heavy chronic and binge drinking are highest steatosis), which is relatively benign, generally revers- among 18–25 year olds. With increasing age, alcohol abuse ible, and associated with hepatocellular accumulations of rates decline and are 50–60 % lower among individuals lipids, principally triglycerides. Stage 2, steatohepatitis, who are 26 years and older compared with the 18–25-year- develops in the setting of hepatic steatosis and is associated old bracket. On the other hand, the soaring rates of heavy with organelle dysfunction, oxidative stress, hepatocellular drinking among teens and even younger minors are dis- injury, and inflammation. Steatohepatitis is a disease state concerting, particularly because both long- and short-term that is triggered by complex interactive hepatotoxic effects consequences of extreme under-age drinking threaten physi- of acetaldehyde, NADH, and reactive oxygen species cal health, mental health, and socioeconomic well-being. (ROS), together with lipotoxicity, endoplasmic reticulum Correspondingly, in adolescents and young adults, chronic (ER) stress, proinflammatory cytokine activation, and/or heavy and binge drinking increase for subsequently meeting gut endotoxin-mediated injury [40, 88, 122, 151]. Stage 3 DSM-IV criteria for alcohol dependence, and subsequently reflects progression of steatohepatitis from a predominantly developing neurocognitive impairment and neurodegenera- inflammatory and injury state to a stage where hepatocel- tion with deficits in learning, memory, and executive func- lular regeneration and repair are severely compromised and tions. This article reviews the nature of acute and chronic fibrogenesis begins to dominate, further limiting metabolic alcohol-mediated neuropathologic lesions, including vulner- and homeostatic functions of the liver [5, 48]. Chronic, pro- able targets of injury in the nervous system. gressive alcohol-induced liver injury increases risk for cir- rhosis and hepatocellular carcinoma [51]. Alcohol metabolism and toxins Mediators of acute alcohol-related encephalopathy Alcohol (ethanol) is absorbed in the upper gastrointestinal tract by diffusion, and then rapidly distributes to all organs. Alcohol abuse has acute and chronic adverse effects on Alcohol is eliminated primarily by oxidation in the liver brain structure and function. Secondary injuries such as 1 3 Acta Neuropathol (2014) 127:71–90 73 contusions and stroke are not considered in this review. diseases remains unresolved, probably due to overlap in Alcohol’s toxic/metabolic effects on the brain are mediated their effects, combined with the fact that alcohol impairs by hepatic encephalopathy, as well
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