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Interactions Between Chronic Ethanol Consumption and Thiamine Deficiency on Neural Plasticity, Spatial Memory, and Cognitive Flexibility.
- Source :
- Alcoholism: Clinical & Experimental Research; Nov2015, Vol. 39 Issue 11, p2143-2153, 11p
- Publication Year :
- 2015
-
Abstract
- Background Many alcoholics display moderate to severe cognitive dysfunction accompanied by brain pathology. A factor confounded with prolonged heavy alcohol consumption is poor nutrition, and many alcoholics are thiamine deficient. Thus, thiamine deficiency ( TD) has emerged as a key factor underlying alcohol-related brain damage ( ARBD). TD in humans can lead to Wernicke Encephalitis that can progress into Wernicke-Korsakoff syndrome and these disorders have a high prevalence among alcoholics. Animal models are critical for determining the exact contributions of ethanol (EtOH)- and TD-induced neurotoxicity, as well as the interactions of those factors to brain and cognitive dysfunction. Methods Adult rats were randomly assigned to 1 of 6 treatment conditions: chronic EtOH treatment ( CET) where rats consumed a 20% v/v solution of EtOH over 6 months; severe pyrithiamine-induced TD ( PTD-moderate acute stage); moderate PTD ( PTD-early acute stage); moderate PTD followed by CET ( PTD- CET); moderate PTD during CET ( CET- PTD); and pair-fed (PF) control. After recovery from treatment, all rats were tested on spontaneous alternation and attentional set-shifting. After behavioral testing, brains were harvested for determination of mature brain-derived neurotrophic factor ( BDNF) and thalamic pathology. Results Moderate TD combined with CET, regardless of treatment order, produced significant impairments in spatial memory, cognitive flexibility, and reductions in brain plasticity as measured by BDNF levels in the frontal cortex and hippocampus. These alterations are greater than those seen in moderate TD alone, and the synergistic effects of moderate TD with CET lead to a unique cognitive profile. However, CET did not exacerbate thalamic pathology seen after moderate TD. Conclusions These data support the emerging theory that subclinical TD during chronic heavy alcohol consumption is critical for the development of significant cognitive impairment associated with ARBD. [ABSTRACT FROM AUTHOR]
- Subjects :
- COMPLICATIONS of alcoholism
ANALYSIS of variance
ANIMAL behavior
ANIMAL experimentation
BIOLOGICAL models
COGNITION
STATISTICAL correlation
ENZYME-linked immunosorbent assay
ETHANOL
RESEARCH methodology
MEMORY
NERVE tissue proteins
NEUROPLASTICITY
PYRIDINE
RATS
RESEARCH funding
STATISTICAL sampling
THALAMUS
TISSUE culture
VITAMIN B1
VITAMIN B1 deficiency
REPEATED measures design
DATA analysis software
DESCRIPTIVE statistics
DISEASE complications
Subjects
Details
- Language :
- English
- Volume :
- 39
- Issue :
- 11
- Database :
- Complementary Index
- Journal :
- Alcoholism: Clinical & Experimental Research
- Publication Type :
- Academic Journal
- Accession number :
- 110546911
- Full Text :
- https://doi.org/10.1111/acer.12859