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Query: UMLS:C0153640 (Cerebellum)
 1,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is generally believed that chronic alcohol consumption results in cerebellar atrophy and Purkinje cell loss, especially in the anterior vermal region. A post-mortem stereological design was applied to cerebella from 10 chronic male alcoholics (mean age 45.5 years) with a minimum of 10 years of severe addiction and 10 male controls (mean age 42.5 years). All alcoholics had pathoanatomical evidence of alcohol abuse but no clinical signs of Wernicke's encephalopathy. Cerebellum was divided into five different areas: the anterior and posterior lobe, the anterior and posterior vermis, and the flocculonodular lobe. The total cortex and white matter volume, the cerebellar surface area, the total Purkinje and granule cell number and density, and the mean volume of Purkinje cells and their cell nuclei were measured in all five regions using stereological methods. The volume of the granular layer was increased by 13% with an increase in layer thickness by 17% possibly due to oedema. Globally, the mean volume of the Purkinje cell perikaryon was decreased by 24% with a decrease in the volume of Purkinje cell nuclei by 16%. The increase of the granular layer and the decrease of Purkinje cell size resulted in a 21% global reduction of Purkinje cell density without a concomitant loss of neurons. No significant regional or global cortical and white matter atrophy was found in cerebella from alcoholics compared to controls.
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PMID:Reduction of Purkinje cell volume in cerebellum of alcoholics. 1506 31

Previous studies have reported cerebellar abnormalities or static ataxia associated with risk for chronic use of alcohol and drugs. Adverse childhood experience is another strong risk factor for later substance abuse. We therefore sought to ascertain the relationship between morphological phenotypes of the lingula (lobule I) of the anterior cerebellar vermis, and exposure to emotional (EM) versus physical (PM) maltreatment, on the degree of ongoing alcohol or drug use. The study design consisted of a cross-sectional in vivo neuroimaging study, utilizing retrospective assessment of maltreatment history and self-reports of alcohol and substance use. Study participants were 153 subjects (54 M/99F, 21.9 +/- 2.2 years) selected for imaging from a database of 1,402 community participants 18-25 years of age, who completed a detailed online screening instrument and met rigorous inclusion/exclusion criteria. Subjects were exposed to only physical abuse or harsh corporal punishment (HCP; PM group, n = 37) and parental verbal abuse and/or witnessing domestic violence (EM group, n = 58) or had no history of maltreatment or axis I disorders (n = 58). The main outcome measures consisted of the gray matter volume of lobule I as measured by manual tracing, number and type of alcoholic beverages consumed during a drinking session, number of sessions per month, and monthly drug use, along with family history of drug and alcohol abuse. Lingula thickness was not attenuated by alcohol use or maltreatment history. However, increased lingula thickness was associated with greater consumption of drugs and hard liquor, particularly in physically maltreated subjects who consumed 2.5- and 2.7-fold more alcohol and used drugs 6.1- and 7.8-fold more frequently than controls or EM subjects, respectively. In conclusion, physical maltreatment was observed to interact with cerebellar morphology resulting in a strong association with alcohol and substance use. Lingula thickness may represent a novel, experientially sensitive, phenotypic risk factor for enhanced alcohol and drug use that perhaps modulates sensitivity to these agents.
Cerebellum 2010 Jun
PMID:Cerebellar lingula size and experiential risk factors associated with high levels of alcohol and drug use in young adults. 2040 61

Alcohol abuse causes cerebellar dysfunction and cerebellar ataxia is a common feature in alcoholics. Alcohol exposure during development also impacts the cerebellum. Children with fetal alcohol spectrum disorder (FASD) show many symptoms associated specifically with cerebellar deficits. However, the cellular and molecular mechanisms are unclear. This special issue discusses the most recent advances in the study of mechanisms underlying alcoholinduced cerebellar deficits. The alteration in GABAA receptor-dependent neurotransmission is a potential mechanism for ethanol-induced cerebellar dysfunction. Recent advances indicate ethanol-induced increases in GABA release are not only in Purkinje cells (PCs), but also in molecular layer interneurons and granule cells. Ethanol is shown to disrupt the molecular events at the mossy fiber - granule cell - Golgi cell (MGG) synaptic site and granule cell parallel fibers - PCs (GPP) synaptic site, which may be responsible for ethanol-induced cerebellar ataxia. Aging and ethanol may affect the smooth endoplasmic reticulum (SER) of PC dendrites and cause dendritic regression. Ethanol withdrawal causes mitochondrial damage and aberrant gene modifications in the cerebellum. The interaction between these events may result in neuronal degeneration, thereby contributing to motoric deficit. Ethanol activates doublestranded RNA (dsRNA)-activated protein kinase (PKR) and PKR activation is involved ethanolinduced neuroinflammation and neurotoxicity in the developing cerebellum. Ethanol alters the development of cerebellar circuitry following the loss of PCs, which could result in modifications of the structure and function of other brain regions that receive cerebellar inputs. Lastly, choline, an essential nutrient is evaluated for its potential protection against ethanol-induced cerebellar damages. Choline is shown to ameliorate ethanol-induced cerebellar dysfunction when given before ethanol exposure.
Cerebellum 2015 Aug
PMID:Effects of Ethanol on the Cerebellum: Advances and Prospects. 2593 48