Animal Models of Alcohol-Induced Dementia

Ribeiro, Ângela Maria; Pereira, Simone Cardoso Lisboa

doi:10.1007/978-1-60761-898-0_33

Cited by 2 publications

(3 citation statements)

References 113 publications

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“…These include loss of cells in the basal forebrain, hippocampal acetylcholine hypofunction, and shrinkage of frontal grey and white matter, with thiamine deficiency characterized by additional lesions in the diencephalon [27]. Vetreno and colleagues [27] suggested that the interaction between ethanol and thiamine deficiency does not produce more behavioral or neural pathology, with the exception of reduced white matter, than long -term thiamine deficiency alone; however, synergic effects have been noted elsewhere [28]. Notably, pure cases of thiamine deficiency, unaccompanied by chronic and excessive alcohol consumption (such as in cases of malnutrition), show a low rate of progression to KS [29], giving credence to the idea that an interaction of causative factors is responsible for the lasting cognitive deficits seen in alcohol-related disorders.…”

Section: The Relationship Of Wernicke-korsakoff Syndrome To Alcohol-rmentioning

confidence: 99%

“…These clinical findings are consistent with current neuroimaging evidence that suggests the possibility of at least partial structural and functional recovery from alcohol-related brain damage if abstinence is maintained. A recent animal study reported that while the effects of chronic ethanol exposure (including working memory and episodic memory impairment) can recover with prolonged abstinence, the deficits of thiamine deficiency (spatial memory impairment and increased perseverative behavior) are more persistent [28]. …”

Section: Neuropsychological Findingsmentioning

confidence: 99%

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Alcohol-related dementia: an update of the evidence

Ridley

Draper

Withall

2013

Alzheimers Res Ther

235

224

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The characteristics of dementia relating to excessive alcohol use have received increased research interest in recent times. In this paper, the neuropathology, nosology, epidemiology, clinical features, and neuropsychology of alcohol-related dementia (ARD) and alcohol-induced persisting amnestic syndrome (Wernicke-Korsakoff syndrome, or WKS) are reviewed. Neuropathological and imaging studies suggest that excessive and prolonged use of alcohol may lead to structural and functional damage that is permanent in nature; however, there is debate about the relative contributions of the direct toxic effect of alcohol (neurotoxicity hypothesis), and the impact of thiamine deficiency, to lasting damage. Investigation of alcohol-related cognitive impairment has been further complicated by differing definitions of patterns of alcohol use and associated lifestyle factors related to the abuse of alcohol. Present diagnostic systems identify two main syndromes of alcohol-related cognitive impairment: ARD and WKS. However, 'alcohol-related brain damage' is increasingly used as an umbrella term to encompass the heterogeneity of these disorders. It is unclear what level of drinking may pose a risk for the development of brain damage or, in fact, whether lower levels of alcohol may protect against other forms of dementia. Epidemiological studies suggest that individuals with ARD typically have a younger age of onset than those with other forms of dementia, are more likely to be male, and often are socially isolated. The cognitive profile of ARD appears to involve both cortical and subcortical pathology, and deficits are most frequently observed on tasks of visuospatial function as well as memory and higher-order (executive) tasks. The WKS appears more heterogeneous in nature than originally documented, and deficits on executive tasks commonly are reported in conjunction with characteristic memory deficits. Individuals with alcohol-related disorders have the potential to at least partially recover - both structurally and functionally - if abstinence is maintained. In this review, considerations in a clinical setting and recommendations for diagnosis and management are discussed.

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Section: The Relationship Of Wernicke-korsakoff Syndrome To Alcohol-rmentioning

confidence: 99%

Section: Neuropsychological Findingsmentioning

confidence: 99%

Alcohol-related dementia: an update of the evidence

Ridley

Draper

Withall

2013

Alzheimers Res Ther

235

224

View full text Add to dashboard Cite

show abstract

“…There still are conflicting opinions about the pathogenesis of KS, with much of the debate revolving around the relative contributions of nutritional deficiency and alcohol neurotoxicity (Ribeiro and Pereira 2010). In any case, it should be noted that Korsakoff’s own account of the neuropathology of the syndrome also included damage to large regions of the brain, including cerebral cortex and structures deep within the brain; however precise cortical and subcortical loci were not detailed (Victor and Yakovlev 1955).…”

Section: Introductionmentioning

confidence: 99%

Function and Dysfunction of Prefrontal Brain Circuitry in Alcoholic Korsakoff’s Syndrome

Oscar‐Berman

2012

Neuropsychol Rev

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The signature symptom of alcohol-induced persisting amnestic disorder, more commonly referred to as alcoholic Korsakoff’s syndrome (KS), is anterograde amnesia, or memory loss for recent events, and until the mid 20th Century, the putative brain damage was considered to be in diencephalic and medial temporal lobe structures. Overall intelligence, as measured by standardized IQ tests, usually remains intact. Preservation of IQ occurs because memories formed before the onset of prolonged heavy drinking — the types of information and abilities tapped by intelligence tests — remain relatively well preserved compared with memories recently acquired. However, clinical and experimental evidence has shown that neurobehavioral dysfunction in alcoholic patients with KS does include nonmnemonic abilities, and further brain damage involves extensive frontal and limbic circuitries. Among the abnormalities are confabulation, disruption of elements of executive functioning and cognitive control, and emotional impairments. Here, we discuss the relationship between neurobehavioral impairments in KS and alcoholism-related brain damage. More specifically, we examine the role of damage to prefrontal brain systems in the neuropsychological profile of alcoholic KS.

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Animal Models of Alcohol-Induced Dementia

Cited by 2 publications

References 113 publications

Alcohol-related dementia: an update of the evidence

Alcohol-related dementia: an update of the evidence

Function and Dysfunction of Prefrontal Brain Circuitry in Alcoholic Korsakoff’s Syndrome

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