Rasagiline prevents neurodegeneration in thiamine deficient rats—A longitudinal MRI study

Dror, Vered; Rehavi, Moshe; Biton, Inbal E.; Eliash, Sarah

doi:10.1016/j.brainres.2013.12.030

Cited by 12 publications

(7 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings in the PE group are consistent with enlargement of lateral ventricles observed with MRI in thiamine deficient rats (i.e., equivalent to the PS group in this study)(Dror et al 2010; Dror et al 2014; Zahr et al 2014a). In the previous studies, however, ventricular enlargement was more profound and appeared to persist (Dror et al 2010; Dror et al 2014), possibly because the length of thiamine deficiency was longer (14 days) and thiamine replacement was shorter (3 days)(Dror et al 2010; Dror et al 2014). Although the TE group did not show statistically significant group effects, lateral ventricle and total CSF volumes were enlarged following the first EtOH exposure period.…”

Section: Discussionsupporting

confidence: 91%

Concomitants of alcoholism: differential effects of thiamine deficiency, liver damage, and food deprivation on the rat brain in vivo

et al. 2016

View full text Add to dashboard Cite

Rationale Serious neurological concomitants of alcoholism include Wernicke's Encephalopathy (WE), Korsakoff's Syndrome (KS) and hepatic encephalopathy (HE). Objectives This study was conducted in animal models to determine neuroradiological signatures associated with liver damage caused by carbon tetrachloride (CCl4), thiamine deficiency caused by pyrithiamine treatment, and nonspecific nutritional deficiency caused by food deprivation. Methods Magnetic resonance imaging (MRI) and spectroscopy (MRS) were used to evaluate brains of wild-type Wistar rats at baseline and following treatment. Results Similar to observations in ethanol (EtOH) exposure models, thiamine deficiency caused enlargement of the lateral ventricles. Liver damage was not associated with effects on cerebrospinal fluid volumes, whereas food deprivation caused modest enlargement of the cisterns. In contrast to what has repeatedly been shown in EtOH exposure models, in which levels of choline-containing compounds (Cho) measured by MRS are elevated, Cho levels in treated animals in all 3 experiments (i.e., liver damage, thiamine deficiency, food deprivation) were lower than baseline or controls. Conclusions These results add to the growing body of literature suggesting that MRS-detectable Cho is labile and can depend on a number of variables that are not often considered in human experiments. These results also suggest that reductions in Cho observed in humans with alcohol use disorder (AUD) may well be due to mild manifestations of concomitants of AUD such as liver damage or nutritional deficiencies and not necessarily to alcohol consumption per se.

show abstract

Section: Discussionsupporting

confidence: 91%

Concomitants of alcoholism: differential effects of thiamine deficiency, liver damage, and food deprivation on the rat brain in vivo

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Although previous work has not directly examined the relationship between plasma phospholipid PUFAs and white matter microstructure of the fornix, several lines of evidence support this finding. Various diets and dietary components, including the Mediterranean diet (38), PUFAs (3,34), vitamin E (3), vitamin D (39), vitamin B1 (40), and vitamin B12 (41) have been linked to white matter integrity. The fornix in particular is vulnerable to the white matter atrophy induced by Alzheimer’s pathology (42).…”

Section: Discussionmentioning

confidence: 99%

Predictors of Memory in Healthy Aging: Polyunsaturated Fatty Acid Balance and Fornix White Matter Integrity

Zamroziewicz¹,

Paul²,

Zwilling³

et al. 2017

Aging and disease

View full text Add to dashboard Cite

Recent evidence demonstrates that age and disease-related decline in cognition depends not only upon degeneration in brain structure and function, but also on dietary intake and nutritional status. Memory, a potential preclinical marker of Alzheimer’s disease, is supported by white matter integrity in the brain and dietary patterns high in omega-3 and omega-6 polyunsaturated fatty acids. However, the extent to which memory is supported by specific omega-3 and omega-6 polyunsaturated fatty acids, and the degree to which this relationship is reliant upon microstructure of particular white matter regions is not known. This study therefore examined the cross-sectional relationship between empirically-derived patterns of omega-3 and omega-6 polyunsaturated fatty acids (represented by nutrient biomarker patterns), memory, and regional white matter microstructure in healthy, older adults. We measured thirteen plasma phospholipid omega-3 and omega-6 polyunsaturated fatty acids, memory, and regional white matter microstructure in 94 cognitively intact older adults (65 to 75 years old). A three-step mediation analysis was implemented using multivariate linear regressions, adjusted for age, gender, education, income, depression status, and body mass index. The mediation analysis revealed that a mixture of plasma phospholipid omega-3 and omega-6 polyunsaturated fatty acids is linked to memory and that white matter microstructure of the fornix fully mediates the relationship between this pattern of plasma phospholipid polyunsaturated fatty acids and memory. These results suggest that memory may be optimally supported by a balance of plasma phospholipid omega-3 and omega-6 polyunsaturated fatty acids through the preservation of fornix white matter microstructure in cognitively intact older adults. This report provides novel evidence for the benefits of plasma phospholipid omega-3 and omega-6 polyunsaturated fatty acid balance on memory and underlying white matter microstructure.

show abstract

“…Beriberi was thought of as a disease of the peripheral nervous system, heart, and muscles until the 1930s when it was found that Wernicke’s encephalopathy was the acute cerebral manifestation of severe thiamin deficiency[24]. In humans, the neurological disorder that is most clearly associated with TD is Wernicke-Korsakoff syndrome (WKS), characterized by behavioral, cognitive and neuropathological deficits [25]. Administration of thiamine is able to prevent, reduce or reverse several symptoms in WKS patients, whereas some deficits persist permanently [26].…”

Section: Introductionmentioning

confidence: 99%

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

2016

View full text Add to dashboard Cite

Thiamine (Vitamin B1) is an essential nutrient and indispensable for normal growth and development of the organism due to its multilateral participation in key biochemical and physiological processes. Humans must obtain thiamine from their diet since it is synthesized only in bacteria, fungi and plants. Thiamine deficiency (TD) can result from inadequate intake, increased requirement, excessive deletion and chronic alcohol consumption. TD affects multiple organ systems, including the cardiovascular, muscular, gastrointestinal, and central and peripheral nervous systems. In the brain, TD causes a cascade of events including mild impairment of oxidative metabolism, neuroinflammation and neurodegeneration, which are commonly observed in neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Thiamine metabolites may serve as promising biomarkers for neurodegenerative diseases and thiamine supplementations exhibit therapeutic potential for patients of some neurodegenerative diseases. Experimental TD has been used to model aging-related neurodegenerative diseases. However, to date, the cellular and molecular mechanisms underlying TD-induced neurodegeneration are not clear. Recent research evidence indicates that TD causes oxidative stress, endoplasmic reticulum (ER) stress and autophagy in the brain, which are known to contribute to the pathogenesis of various neurodegenerative diseases. In this review, we discuss the role of oxidative stress, ER stress and autophagy in TD-mediated neurodegeneration. We propose that it is the interplay of oxidative stress, ER stress and autophagy that contributes to TD-mediated neurodegeneration.

show abstract

Rasagiline prevents neurodegeneration in thiamine deficient rats—A longitudinal MRI study

Cited by 12 publications

References 40 publications

Concomitants of alcoholism: differential effects of thiamine deficiency, liver damage, and food deprivation on the rat brain in vivo

Concomitants of alcoholism: differential effects of thiamine deficiency, liver damage, and food deprivation on the rat brain in vivo

Predictors of Memory in Healthy Aging: Polyunsaturated Fatty Acid Balance and Fornix White Matter Integrity

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

Contact Info

Product

Resources

About