Relevant bibliographies by topics / Brain Alcoholism Alcohol

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Brain Alcoholism Alcohol'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Brain Alcoholism Alcohol"

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Lishman, W. A. "Alcohol and the Brain." British Journal of Psychiatry 156, no. 5 (May 1990): 635–44. http://dx.doi.org/10.1192/bjp.156.5.635.

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Some of the major effects of alcohol, and alcoholism, on the brain are reviewed, with reappraisal of evidence drawn from brain imaging, neuropathology, clinical psychology, and laboratory experimental work. A hypothesis is developed which may help to account for the wide variability encountered in individual susceptibility to alcoholic brain damage and its varied manifestations. Therapeutic implications are considered.
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Le Berre, A. P., G. Rauchs, R. La Joie, F. Mézenge, C. Boudehent, F. Vabret, S. Segobin, et al. "Impaired decision-making and brain shrinkage in alcoholism." European Psychiatry 29, no. 3 (March 2014): 125–33. http://dx.doi.org/10.1016/j.eurpsy.2012.10.002.

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AbstractAlcohol-dependent individuals usually favor instant gratification of alcohol use and ignore its long-term negative consequences, reflecting impaired decision-making. According to the somatic marker hypothesis, decision-making abilities are subtended by an extended brain network. As chronic alcohol consumption is known to be associated with brain shrinkage in this network, the present study investigated relationships between brain shrinkage and decision-making impairments in alcohol-dependent individuals early in abstinence using voxel-based morphometry. Thirty patients performed the Iowa Gambling Task and underwent a magnetic resonance imaging investigation (1.5T). Decision-making performances and brain data were compared with those of age-matched healthy controls. In the alcoholic group, a multiple regression analysis was conducted with two predictors (gray matter [GM] volume and decision-making measure) and two covariates (number of withdrawals and duration of alcoholism). Compared with controls, alcoholics had impaired decision-making and widespread reduced gray matter volume, especially in regions involved in decision-making. The regression analysis revealed links between high GM volume in the ventromedial prefrontal cortex, dorsal anterior cingulate cortex and right hippocampal formation, and high decision-making scores (P < 0.001, uncorrected). Decision-making deficits in alcoholism may result from impairment of both emotional and cognitive networks.
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Kashem, Mohammed Abul, Omar Šerý, David V. Pow, Benjamin D. Rowlands, Caroline D. Rae, and Vladimir J. Balcar. "Actions of Alcohol in Brain: Genetics, Metabolomics, GABA Receptors, Proteomics and Glutamate Transporter GLAST/EAAT1." Current Molecular Pharmacology 14, no. 2 (December 31, 2020): 138–49. http://dx.doi.org/10.2174/1874467213666200424155244.

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We present an overview of genetic, metabolomic, proteomic and neurochemical studies done mainly in our laboratories that could improve prediction, mechanistic understanding and possibly extend to diagnostics and treatment of alcoholism and alcohol addiction. Specific polymorphisms in genes encoding for interleukins 2 and 6, catechol-O-methyl transferase (COMT), monaminooxidase B (MAO B) and several other enzymes were identified as associated with altered risks of alcoholism in humans. A polymorphism in the gene for BDNF has been linked to the risk of developing deficiences in colour vision sometimes observed in alcoholics. Metabolomic studies of acute ethanol effects on guinea pig brain cortex in vitro, lead to the identification of specific subtypes of GABA(A) receptors involved in the actions of alcohol at various doses. Acute alcohol affected energy metabolism, oxidation and the production of actaldehyde and acetate; this could have specific consequences not only for the brain energy production/utilization but could influence the cytotoxicity of alcohol and impact the epigenetics (histone acetylation). It is unlikely that brain metabolism of ethanol occurs to any significant degree; the reduction in glucose metabolism following alcohol consumption is due to ethanol effects on receptors, such as α4β3δ GABA(A) receptors. Metabolomics using post-mortem human brain indicated that the catecholaminergic signalling may be preferentially affected by chronic excessive drinking. Changes in the levels of glutathione were consistent with the presence of severe oxidative stress. Proteomics of the post-mortem alcoholic brains identified a large number of proteins, the expression of which was altered by chronic alcohol, with those associated with brain energy metabolism among the most numerous. Neurochemical studies found the increased expression of glutamate transporter GLAST/EAAT1 in brain as one of the largest changes caused by alcoholism. Given that GLAST/EAAT1 is one of the most abundant proteins in the nervous tissue and is intimately associated with the function of the excitatory (glutamatergic) synapses, this may be among the most important effects of chronic alcohol on brain function. It has so far been observed mainly in the prefrontal cortex. We show several experiments suggesting that acute alcohol can translocate GLAST/EAAT1 in astrocytes towards the plasma membrane (and this effect is inhibited by the GABA(B) agonist baclofen) but neither the mechanism nor the specificity (to alcohol) of this phenomenon have been established. Furthermore, as GLAST/EAAT1 is also expressed in testes and sperm (and could also be affected there by chronic alcohol), the levels of GLAST/EAAT1 in sperm could be used as a diagnostic tool in testing the severity of alcoholism in human males. We conclude that the reviewed studies present a unique set of data which could help to predict the risk of developing alcohol dependence (genetics), to improve the understanding of the intoxicating actions of alcohol (metabolomics), to aid in assessing the extent of damage to brain cells caused by chronic excessive drinking (metabolomics and proteomics) and to point to molecular targets that could be used in the treatment and diagnosis of alcoholism and alcohol addiction.
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Ragan, Paul W., Charles K. Singleton, and Peter R. Martin. "Brain Injury Associated With Chronic Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 66–68. http://dx.doi.org/10.1017/s1092852900011226.

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AbstractAlcoholism can result in a number of severe consequences to the central nervous system, including Korsakoff's psychosis, delusions, delirium, Wernicke's encephalopathy, and cerebellar degeneration. Many of these disorders have a substantially higher prevalence than had been previously believed. Neuropathologic and neuroimaging studies have been instrumental in identifying the changes undergone by the alcoholic brain and the factors that may contribute to alcohol-induced brain damage. Biologic differences appear to make women especially susceptible to central nervous system insult from alcohol abuse. The damage caused by alcohol may be associated, in part, with thiamine deficiency, neuronal excitotoxicity, and magnesium wasting.
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Hayakawa, K., H. Kumagai, Y. Suzuki, N. Furusawa, T. Haga, T. Hoshi, Y. Fujiwara, and K. Yamaguchi. "Mr Imaging of Chronic Alcoholism." Acta Radiologica 33, no. 3 (May 1992): 201–6. http://dx.doi.org/10.1177/028418519203300302.

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We evaluated the brain lesions of patients with chronic alcoholism (n = 34) in comparison with age- and sex-matched controls (n = 40) by MR imaging. T1-weighted sagittal and axial images and T2-weighted axial images were obtained with a 0.5 T superconducting MR unit. Various brain measurements were then performed, and the presence of regions of abnormal signal intensity was also compared between the two groups. The brain measurements revealed significant cerebral atrophy (characterized by lateral and 3rd ventricular dilatation, and widening of the interhemispheric fissure) as well as significant cerebellar atrophy (represented by 4th ventricular dilatation) in the alcoholic group. These changes were more prominent in patients in their fifties and sixties than in those aged in the thirties and forties. Focal hypointense lesions were observed in 20.6% of the alcoholics and in 5% of the controls (p < 0.01), while focal hyperintense lesions were observed in 61.8% of the alcoholics and in 20% of the controls (p < 0.001). The severity of these MR findings correlated well with the age of the patients. These observations suggest that alcohol is an important promotor of brain aging.
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Shri, T. K. Padma, and N. Sriraam. "EEG Based Detection of Alcoholics." International Journal of Biomedical and Clinical Engineering 1, no. 1 (January 2012): 59–76. http://dx.doi.org/10.4018/ijbce.2012010105.

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The short term and long term effects of alcohol on various organs of the body, especially on the human brain is well established by numerous studies. Invasive methods such as Transcranial Magnetic Stimulation (TMS) and non invasive imaging techniques such as Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Positron Emission Tomography (PET), and functional MRI activated electro-encephalogram (EEG) have been used to study the changes in EEG activity due to alcoholism. Even with the advent of neuro imaging techniques, EEG happens to be an important tool for brain study providing a non- invasive and cost effective method to detect the effects of alcohol on the human brain. This paper discusses the harmful effects of alcohol on different organs of the body. The advances in the development of EEG signal processing algorithms over the past decade for alcoholic detection are reviewed and their limitations are reported. Further the use of EEG for mass screening of alcoholics and biometric application is discussed in detail.
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Brenner, Eric, Gayatri R. Tiwari, Manav Kapoor, Yunlong Liu, Amy Brock, and R. Dayne Mayfield. "Single cell transcriptome profiling of the human alcohol-dependent brain." Human Molecular Genetics 29, no. 7 (March 6, 2020): 1144–53. http://dx.doi.org/10.1093/hmg/ddaa038.

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Abstract Alcoholism remains a prevalent health concern throughout the world. Previous studies have identified transcriptomic patterns in the brain associated with alcohol dependence in both humans and animal models. But none of these studies have systematically investigated expression within the unique cell types present in the brain. We utilized single nucleus RNA sequencing (snRNA-seq) to examine the transcriptomes of over 16 000 nuclei isolated from the prefrontal cortex of alcoholic and control individuals. Each nucleus was assigned to one of seven major cell types by unsupervised clustering. Cell type enrichment patterns varied greatly among neuroinflammatory-related genes, which are known to play roles in alcohol dependence and neurodegeneration. Differential expression analysis identified cell type-specific genes with altered expression in alcoholics. The largest number of differentially expressed genes (DEGs), including both protein-coding and non-coding, were detected in astrocytes, oligodendrocytes and microglia. To our knowledge, this is the first single cell transcriptome analysis of alcohol-associated gene expression in any species and the first such analysis in humans for any addictive substance. These findings greatly advance the understanding of transcriptomic changes in the brain of alcohol-dependent individuals.
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Kuruoglu, Asli Çepik, Zehra Arikan, Gülin Vural, Metin Karataş, Mehmet Araç, and Erdal Işik. "Single Photon Emission Computerised Tomography in Chronic Alcoholism." British Journal of Psychiatry 169, no. 3 (September 1996): 348–54. http://dx.doi.org/10.1192/bjp.169.3.348.

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BackgroundWe examined the functional and structural cerebral changes in chronic alcoholics, analysing their association with personality features and alcohol drinking habits.MethodForty patients with alcohol dependency, including 15 with antisocial personality disorder (ASP) as defined in DSM–III–R and 10 age and sex matched healthy controls were studied after termination of withdrawal symptoms, using high resolution single photon emission tomography (SPECT), cranial computerised tomography (CT) and brainstem auditory evoked potentials (BAEP).ResultsWe found significant reductions in regional cerebral blood flow (rCBF) measurements of alcoholic patients. Low flow in frontal regions encountered in 67.5% of the patients was associated with the duration of alcohol consumption, while no such relation existed with the amount of daily intake. Patients with ASP exhibited more marked frontal hypoperfusion. Significant brain atrophy detected by CT was present in 40% of the patients and did not correlate with frontal hypoperfusion.ConclusionsPatients with ASP are more sensitive to toxic effects of alcohol. Alternatively chronic alcoholism leads to frontal lobe dysfunction recognised as ASP in the clinical setting.
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Jacobson, R. R., and W. A. Lishman. "Cortical and diencephalic lesions in Korsakoff's syndrome: a clinical and scan study." Psychological Medicine 20, no. 1 (February 1990): 63–75. http://dx.doi.org/10.1017/s0033291700013234.

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SYNOPSISTwenty-five male alcoholic Korsakoff patients were compared with age and sex-matched non-Korsakoff chronic alcoholics and healthy volunteers on clinical and CT brain scan parameters. The scans were assessed by planimetry, visual grading procedures and computerized analysis. Reliable measures of third ventricular size were developed.The Korsakoff patients had wider third ventricles, larger lateral ventricles and wider interhemispheric fissures than the comparison groups; but sulcal and Sylvian fissure widths were equivalent in Korsakoff and non-Korsakoff alcoholics.The results suggest that, in addition to their well-established diencephalic lesions, many Korsakoff patients have sustained widespread cerebral damage. Shrinkage in the frontal brain regions appears to be especially pronounced. The implications for a dual aetiology of alcoholic Korsakoff's syndrome involving thiamine deficiency and features associated with alcoholism, probably direct alcohol neurotoxicity, are discussed.
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Koob, George F., and Amanda J. Roberts. "Brain Reward Circuits in Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 23–37. http://dx.doi.org/10.1017/s1092852900011196.

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AbstractThis article discusses the neurocircuitry and the neurochemical systems, as well as the molecular elements within these systems, that are believed to be important in the etiology of alcoholism. Alcoholism is a complex behavioral disorder characterized by excessive consumption of alcohol; a narrowing of the behavioral repertoire toward excessive consumption; the development of tolerance and dependence; and impairment in social and occupational functioning. Animal models of the complete syndrome of alcoholism are difficult if not impossible to achieve, but validated animal models exist for many of the different components of the syndrome.Recent work has begun to define the neurocircuits responsible for the major sources of positive and negative reinforcement that are key to animal models of excessive alcohol intake. Alcohol appears to interact with alcohol-sensitive elements within neuronal membranes that convey the specificity of neurochemical actions. Positive reinforcement appears to be mediated by an activation γ-aminobutyric acid A receptors, release of opioid peptides and dopamine, inhibition of glutamate receptors, and interaction with serotonin systems. These neurocircuits may be altered by chronic alcohol administration. This is reflected by their exhibiting opposite effects during acute alcohol withdrawal, and by the recruitment of other neurotransmitter systems, such as the stress neuropeptide corticotropin-releasing factor. These neuropharmacologic actions are believed to produce allostatic changes in set-point, which set up the vulnerability to relapse that is so characteristic of alcoholism. Future challenges include a focus on understanding exactly how these neuroadaptive changes convey vulnerability to relapse in animals with a history of alcohol dependence.
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Dissertations / Theses on the topic "Brain Alcoholism Alcohol"

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Arlinde, Christina. "Gene expression profiling in animal models of alcoholism /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-133-4/.

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van, der Vaart Andrew D. "Molecular Brain Adaptations to Ethanol: Role of Glycogen Synthase Kinase-3 Beta in the Transition to Excessive Consumption." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5510.

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Alcoholism is a complex neuropsychiatric disease that is characterized by compulsive alcohol use and intensifying cravings and withdrawals, often culminating in physiologic dependency. Fundamental alterations in brain chemistry underlie the transition from initial ethanol exposure to repetitive excessive use. Key mediators of this adaptation include changes in gene expression and signal transduction. Here we investigated gene expression pathways in prefrontal cortex and nucleus accumbens following acute or chronic ethanol treatment, to identify genes with potentially conserved involvement in the long-term response of the corticolimbic system to repeated ethanol exposure. We investigated Gsk3b, which encodes glycogen synthase kinase 3-beta, as a highly ethanol responsive gene associated with risk for long-term maladaptive responses to ethanol. On the level of the protein, we found that GSK3B and to a lesser extent the GSK3A isoform showed robust increases in inhibitory phosphorylation following acute ethanol. This inhibition may underlie aspects of the behavioral response to acute ethanol, as pre-treatment with a GSK3B inhibitor (tideglusib) augmented ethanol’s locomotor effects. Following long term ethanol exposure, we re-tested GSK3B phosphorylation and found that its ethanol response is blunted, consistent with molecular tolerance as a corollary to increased consumption. As the prefrontal cortex (PFC) plays a vital role in the reward pathway via its glutamatergic projections to the nucleus accumbens, we investigated the role of the Gsk3b gene specifically in PFC and in glutamatergic neurons. Overexpression of Gsk3b in the PFC robustly increased ethanol consumption, while deletion in Camk2a-positive neurons significantly attenuated ethanol consumption. Pharmacologic antagonism of GSK3B also decreased drinking in a model of binge-like consumption. Collectively this data implicates GSK3B as a mediator of excessive ethanol intake via its kinase activity, wherein inhibition of the kinase via phosphorylation exerts a protective effect in the context of acute ethanol, but desensitizes with repeated exposure.
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Alexander-Kaufman, Kimberley Louise. "Proteomics of the human alcoholic brain: Implications for the pathophysiology of alcohol-related brain damage." The University of Sydney, 2008. http://hdl.handle.net/2123/2692.

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Doctor of Philosophy (PhD)
Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.
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Hård, Julia. "Långvarigt bruk av alkohol ger kramper och epilepsi : Ett arbete om alkohols effekter på hjärnan." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-65066.

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Alkohol har funnits sedan urminnes tider och är något som de flesta ungdomar och vuxna är bekanta med. Flertalet vet också att för mycket alkohol på lång sikt kan orsaka skador, framförallt på lever (fettlever) och njurar. Men inte alla vet att alkohol skadar hjärnan och kan ge kramper samt epilepsi. Alkohol har olika effekter på kroppen. Akut kan det öka den inhiberande och minska den excitatoriska signaleringen i hjärnan. Långvarigt kan det öka den excitatoriska signaleringen, minska den inhibitoriska samt öka alkoholtoleransen. I hjärnan är balansen mellan den inhibitoriska och excitatoriska signaleringen mycket betydelsefull och rubbningar kan orsaka skador som i sin tur kan orsaka krampanfall. Dessa krampanfall kan bli allvarliga och ibland dödliga. Studier kring sambandet mellan alkohol och epilepsi utförda av Samokhvalov et al. (2010), Devetag et al. (1983), Bråthen et al. (1999), Tartara et al. (1983), Bartolomei et al. (1997), Victor och Brausch (1967) och Hillbom (1980) har visat på olika resultat, men trots skillnaden i resultaten har korrelationen mellan alkohol och epilepsi varit tydlig. I studien av Devetag et al. (1983) hade 58 % av 153 alkoholister anfall icke relaterade till abstinens, alkoholinducering eller sjukdom/skada. Av 60 patienter med krampanfall var 30 stycken (50 %) icke relaterade till abstinens, alkoholinducering eller sjukdom/skada i studien utförd av Bartolomei et al. (1997). Bråthen et al. (1999)  utförde en studie på 142 alkoholister med krampanfall där 16 stycken (36 %) var icke-relaterade till abstinens, alkoholinducering eller sjukdom/skada. Vidare påvisade Tartara et al. (1983) i sin studie 30 patienter med krampanfall där 3 stycken (10 %) inte var relaterade till abstinens, alkohlinducering eller sjukdom/skada. Krampanfall som inte är relaterade till abstinens, akoholinducering eller sjukdom/skada är kluriga och svåra att utreda. Många forskare har försökt få insikt i och reda ut frågan om alkohols influens över utvecklingen av epilepsi och hur det skulle tänkas gå till. När kan alkoholrelaterade krampanfall klassificeras som epilepsi, vad innebär ett alkoholrelaterat krampanfall och vilka orsaker existerar som leder till att sådanan krampanfall uppstår. I den här litteraturstudien utreds kopplingen mellan alkoholism och epilepsi för att bättre förstå sambandet. Till studien har 20 vetenskapliga artiklar använts för att förstå vilka effekter alkohol har på kroppen, vad det innebär att ha epilepsi och hur de båda är kopplade. För att komma fram till ett svar på den framförda frågeställningen i studien, om långvarigt bruk av alkohol ger kramper och epilepsi, användes 7 studier vars undersökingar huvudsakligen fokuserat på alkoholister inlagda med krampanfall. Resultaten från de 7 studierna indikerar sammantaget att alkohol sannolikt kan orsaka epilepsi. Ingen av studierna har visat motsatsen. Långvarigt bruk av alkohol ger kramper och kan även ge epilepsi, men hur det går till är inte klarlagt. Samtidigt finns det många individer som missbrukar alkohol och som inte får epilepsi eller aldrig ens upplever ett enda krampanfall.
Alcohol has been used for drinking for many years and is a substance that is well known to most teenagers and adults. Most people also know that alcohol, when misused, can cause damage to both the liver and the kidneys but not as many people know about the damage alcohol can cause the brain. The damage that alcohol causes in the brain can lead to conditions where the patient can experience seizures, whitch can further devlop into epilepsy. Alcohol has different effects on the body. An immidiate response to alcohol is that the inhibitory signaling in the brain increases and the excitatory signaling decreases. When it comes to a prolonged misuse of alcohol the effects on the brain are the opposite and it can also increase the tolerance for alcohol. Inhibitory and excitatory signaling in the brain are essential and disturbance of those signals can be very damaging to the brain. The damages can develop and become permanent and it can also trigger different kinds of seizures. The seizures can in turn become very serious and fatal. Studies on the connection between alcohol and epilepsy has been conducted by Samokhvalov et al. (2010), Devetag et al. (1983), Bråthen et al. (1999), Tartara et al. (1983), Bartolomei et al. (1997), Victor och Brausch (1967) och Hillbom (1980) and have shown different results. The results however have shown a clear correlation between alcohol and epilepsi. In the study performed by Devetag et al. (1983) 58 % of 153 patients experienced seizures not related to alcohol withdrawl, alcohol induction or injury/disease. Of 60 patients who presented seizures in the study conducted by Bartolomei et al. (1997), 30 (50 %) had seizures not related to alcohol withdrawl, alcohol induction or injury/disease. A study performed by Bråthen et al. (1999) showed  16 patients (36 %) of 142 with seizures not related to alcohol withdrawl, alcohol indiction or injury/disease. Furthermore, a study conducted by Tartara et al. (1983) showed 30 patients with seizures, where 3 (10 %) of them were not related to alcohol withdrawl, alcohol induction or injury/disease. Seizures not related to alcohol withdrawl, alcohol abuse or injury/disease are difficult to investigate. Many scientists have tried to get insight in as to how alcohol can influence the ethiopathogenesis of epilepsy. What is alcohol-related seizures, what is the cause behind the seizures and how does one decide if the seizures can be defines as epilepsy. This literature review investigates the link between alcoholism and epilepsy to better understand this connection. The question of issue was ”if prolonged misuse of alcohol can lead to epilepsy” and to unravel the question, 7 studies were used. The studies main focus was alcoholism and seizures. The results from the studies indicated in total that alcohol prabably can cause epilepsy since none of the studies showed the opposite. A prolonged misuse of alcohol can lead to seizures and even epilepsy, but how this comes to be is not clear and needs to be properly investigated. Not to forget, some people who misuse alcohol do not get epilepsy and some never experience even a single seizure.
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Buckley, Stella Tracey. "GabaA receptor-mediated neurotransmission in human alcoholic brain /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17286.pdf.

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Bazov, Igor. "Epigenetic Dysregulations in the Brain of Human Alcoholics : Analysis of Opioid Genes." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-270321.

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Neuropeptides are special in their expression profiles restricted to neuronal subpopulations and low tissue mRNA levels. Genetic, epigenetic and transcriptional mechanisms that define spatiotemporal expression of the neuropeptide genes have utmost importance for the formation and functions of neural circuits in normal and pathological human brain. This thesis focuses on regulation of transcription of the opioid/nociceptin genes, the largest neuropeptide family, and on identification of adaptive changes in these mechanisms associated with alcoholism as model human pathology. Two epigenetic mechanisms, the common for most cells in the dorsolateral prefrontal cortex (dlPFC) and the neuron-subpopulation specific that may orchestrate prodynorphin (PDYN) transcription in the human dlPFC have been uncovered. The first, repressive mechanism may operate through control of DNA methylation/demethylation in a short, nucleosome size promoter CpG island (CGI). The second mechanism may involve USF2, the sequence–specific methylation–sensitive transcription factor which interaction with its target element in the CpG island results in USF2 and PDYN co-expression in the same neurons. The short PDYN promoter CGI may function as a chromatin element that integrates cellular and environmental signals through changes in methylation and transcription factor binding. Alterations in USF2–dependent PDYN transcription are affected by the promoter SNP (rs1997794: T>C) under transition to pathological state, i.e. in the alcoholic brain. This and two other PDYN SNPs that are most significantly associated with alcoholism represent CpG-SNPs, which are differentially methylated in the human dlPFC. The T, low risk allele of the promoter SNP forms a noncanonical AP-1–binding element. JUND and FOSB proteins, which may form homo- or heterodimers have been identified as dominant constituents of AP-1 complex. The C, non-risk variant of the PDYN 3′ UTR SNP (rs2235749 SNP: C>T) demonstrated significantly higher methylation in alcoholics compared to controls. PDYN mRNA and dynorphin levels significantly and positively correlated with methylation of the PDYN 3′ UTR CpG-SNP suggesting its involvement in PDYN regulation. A DNA–binding factor with differential binding affinity for the T allele and methylated and unmethylated C alleles of the PDYN 3′ UTR SNP (the T allele specific binding factor, Ta-BF) has been discovered, which may function as a regulator of PDYN transcription. These findings emphasize the complexity of PDYN regulation that determines its expression in specific neuronal subpopulations and suggest previously unknown integration of epigenetic, transcriptional and genetic mechanisms that orchestrate alcohol–induced molecular adaptations in the human brain. Given the important role of PDYN in addictive behavior, the findings provide a new insight into fundamental molecular mechanisms of human brain disorder. In addition to PDYN in the dlPFC, the PNOC gene in the hippocampus and OPRL1 gene in central amygdala that were downregulated in alcoholics may contribute to impairment of cognitive control over alcohol seeking and taking behaviour.
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Roy, Arnab. "Evolving spike neural network based spatio-temporal pattern classifiers with an application to identifying the alcoholic brain." Thesis, State University of New York at Binghamton, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3630956.

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We introduce a novel approach to evolving spike neural network (SNN) based Spatio-temporal (ST) pattern classifiers that can detect occurrences of hidden structures in a ST data. We test this learning paradigm to find characteristic electrical patterns in visually evoked response potentials (VERPs) generated by an alcoholic brain.

We cast the alcoholic classification task as a multiple feature selection (FS) problem. The FS problems are grouped under 2 classes: the spatial task and the temporal task. The objective of the spatial FS task is to choose a correct subset of electroencephalogram (EEG) leads (the spatial-features) along with the lead-weighs (numeric attributes) using which a composite signal can be created. The temporal FS task involves detecting temporal patterns that occur more frequently in the alcoholic composite signals than in the control signals. To facilitate the evolution of such a classifier, we introduce design rules for SNN based temporal pattern detectors (TPDs) and novel crossover operators for the simultaneous FS task.

The conventional techniques for characterizing the alcoholic VERPs use the information in the gamma-band (30 to 50 Hz) to develop a set of feature vectors and then train a classifier using these feature vectors. Using the SNN based evolutionary learning paradigm we were able to solve this problem in 1 step; the SNN performed both temporal feature extraction and classification. Unlike the conventional techniques we did not make any specific assumptions regarding the spectral characteristics of the data; we did not implement a gamma-band filter. Also, we located regions on the skull of an alcoholic subject that produced abnormal electrical activity compared to the controls. These regions are consistent with prior findings in the literature. The classification accuracy was measured as the area under the receiver operator characteristic curve (ROC). The area under the ROC curve for the training set varied from 90.32% to 98.83% and for the testing set it varied from 87.17% to 95.9%.

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8

Troni, Kelly Lendini 1980. "Estudo sobre o uso do resíduo da etapa de deceragem de óleo de farelo de arroz para a produção de ácidos graxos e álcoois graxos." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/266628.

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Orientador: Roberta Ceriani
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Engenharia Química
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Resumo: A cera do óleo de farelo de arroz (OFA) é um resíduo da etapa de deceragem no processo de refino de óleos. Tradicionalmente, as ceras naturais, que em excesso geram turbidez no óleo vegetal embalado, são removidas por cristalização e filtração a baixa temperatura. Esse resíduo da etapa de deceragem pode conter de 20 a 80% em massa de óleo, seguido por uma fração principal de ceras, álcoois graxos livres, ácidos graxos livres e hidrocarbonetos. A fração de cera do resíduo é constituída por álcoois graxos e ácidos graxos de cadeia longos esterificados (mais de 18 carbonos). Considerando que o óleo de farelo de arroz tem 4-6% em massa de cera, uma grande quantidade dessa fonte natural de compostos graxos é subaproveitada na indústria de óleos vegetais. De acordo com a revisão bibliográfica, nenhum trabalho na literatura trata da produção de ácidos graxos e de álcoois graxos a partir da hidrólise do resíduo extraído da etapa de deceragem usando vapor supersaturado (elevadas temperaturas e alto vácuo). Nestas condições, a reação de degradação de ceras, ou de desesterificação, ocorre sem a presença de catalisadores em um meio graxo. Diante do exposto, esta dissertação de mestrado teve por objetivo o estudo inédito de aplicação das mesmas condições da desacidificação por via física como rota na produção de ácidos graxos e álcoois graxos a partir do resíduo da etapa de deceragem de óleo de farelo de arroz, sob baixa pressão, a temperaturas elevadas e mediante a injeção de vapor de arraste. Os experimentos foram realizados de acordo com um planejamento fatorial simples (23 + 3 pontos centrais) considerando a temperatura da camisa de aquecimento do vaso do desodorizador (ºC), a vazão de vapor de arraste (mL de água 25 ºC/ min) e o tempo de stripping (min) como variáveis independentes. Os efeitos destas variáveis foram relacionados aos resultados de análises químicas, sendo que, em cada ensaio, foram colhidas amostras para o resíduo e destilado, e analisadas quanto ao teor de ácidos graxos livres, espectros de infravermelho com transformada de Fourier (FTIR), calorimetria exploratória diferencial (DSC) e a técnica EASI-MS (Easy Ambient Sonic- Spray Mass Spectrometry)
Abstract: The rice bran oil wax is a residue of step dewaxing in oil refining process. Traditionally, natural waxes, which generate excessive turbidity in commercial vegetable oil, are removed by crystallization and filtration at low temperatures. This residue of the dewaxing step or winterization may contain from 20 up to 80% by weight of oil, followed by a main fraction of waxes, free fatty alcohols, fatty acids and hydrocarbons. The wax fraction of the residue is composed of esterified fatty alcohols and long-chain fatty acids (more than 18 carbons). Considering that rice bran oil has 4-6% by weight of wax, a large amount of such natural source of fatty compounds is undervalued by the oil industry. According to literature review, no work has reported the production of fatty acids and fatty alcohols from the hydrolysis of the winterization residue using supersaturated steam (high temperatures and high vacuum). Accordingly, the degradation reaction of waxes, or deesterification occurs without the presence of catalysts in an oily medium. Given the above stated, this dissertation aimed to study the unprecedented application of the same conditions as stripping steam deacidification in the production of fatty acids and fatty alcohols from the residue of dewaxing step of rice bran oil, under low pressure, elevated temperatures and with the injection of stripping steam. The experiments were performed according to a simple factorial design (23 + 3 central points), i.e., temperature of the still heating jacket (ºC), the flow of stripping steam (mL water 25 ºC / min) and stripping time (min) as independent variables. The effects of these variables were related to the results of chemical analysis, and in each test, samples were taken for residue and distillate, and analyzed for their content of free fatty acids , spectra of Fourier transform infrared (FTIR), differential scanning calorimetry (DSC) and EASI-MS (Easy-Ambient Sonic Spray Mass Spectrometry)
Mestrado
Desenvolvimento de Processos Químicos
Mestra em Engenharia Química
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Berman, Ari Ethan. "Brain region gene expression responds discretely to chronic alcohol withdrawal with specific disruption of the hippocampus during intoxication." Thesis, 2005. http://hdl.handle.net/2152/2686.

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Liu, Jianwen. "Studies of the global gene expression changes in alcoholic human brain and blood." Thesis, 2005. http://hdl.handle.net/2152/2267.

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Books on the topic "Brain Alcoholism Alcohol"

1

W, Goedde H., ed. Alcohol metabolism, alcohol intolerance, and alcoholism: Biochemical and pharmacogenetic approaches. Berlin: Springer-Verlag, 1990.

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Brennfleck, Shannon Joyce, ed. Alcohol information for teens: Health tips about alcohol and alcoholism : including facts about underage drinking, preventing teen alcohol use, alcohol's effects on the brain and the body, alcohol abuse treatment, help for children of alcoholics, and more. Detroit, MI: Omnigraphics, 2005.

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E, Payne James, ed. Alcohol and the addictive brain: New hope for alcoholics from biogenetic research. New York: Free Press, 1991.

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A, Deitrich Richard, Pawlowski Albert 1925-, National Institute on Alcohol Abuse and Alcoholism (U.S.), and University of Colorado, Boulder. Alcohol Research Center., eds. Initial sensitivity to alcohol: Proceedings of a Workshop on Alcohol Intoxication, October 13-14, 1988, Keystone, Colorado. Rockville, Md. (5600 Fishers Lane, Rockville 20857): The Institute, 1990.

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Organisation of goal-directed behaviour: Development of experimental methods and analysis of chronic and acute effects of alcohol on correlations between brain potentials. Oulu: Universitatis ouluensis, 1994.

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Institute of Medicine (U.S.). Prevention and treatment of alcohol problems: Research opportunities. Washington, D.C: National Academy Press, 1989.

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International, Symposium for Biomedical Research on Alcoholism (1988 Taipei Taiwan). Molecular mechanisms of alcohol: Neurobiology and metabolism. Clifton, N.J: Humana Press, 1989.

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Parker, Philip M., and James N. Parker. Alcohol addiction: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Shannon, Joyce Brennfleck. Alcoholism sourcebook: Basic consumer health information about alcohol use, abuse, and addiction, including facts about the physical consequences of alcohol abuse, such as brain changes and problems with cognitive functioning, cirrhosis and other liver diseases, cardiovascular disease, pancreatitis, and alcoholic neuropathy, and the effects of alcohol on reproductive health and fetal development, mental health problems associated with alcohol abuse, and alcohol's impact on families, workplaces, and the community ; along with information about underage drinking, alcohol treatment and recovery, a glossary of related terms, and directories of resources for more information. 3rd ed. Detroit, MI: Omnigraphics, 2010.

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Nagata, Atsuo. Arukōru no kenkōgaku: Sake o aisuru senmon'i ga oshieru. Tōkyō: Kinokuniya Shoten, 1999.

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Book chapters on the topic "Brain Alcoholism Alcohol"

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Antonow, David R., and Craig J. McClain. "Nutrition and Alcoholism." In Alcohol and the Brain, 81–120. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_4.

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Tarter, Ralph E., and Kathleen L. Edwards. "Neuropsychology of Alcoholism." In Alcohol and the Brain, 217–42. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_8.

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Goldstein, Gerald. "Dementia Associated with Alcoholism." In Alcohol and the Brain, 283–94. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_11.

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Wilkinson, D. Adrian. "Neuroradiologic Investigations of Alcoholism." In Alcohol and the Brain, 183–215. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_7.

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Badawy, Abdulla A. B. "Liver Tryptophan Pyrrolase, Brain 5-Hydroxytryptamine and Alcohol Preference." In Alcoholism, 217–22. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5946-3_23.

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Porjesz, Bernice, and Henri Begleiter. "Human Brain Electrophysiology and Alcoholism." In Alcohol and the Brain, 139–82. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_6.

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Fialkov, M. Jerome. "Biologic and Psychosocial Determinants in the Etiology of Alcoholism." In Alcohol and the Brain, 245–63. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_9.

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Cala, Lesley Ann. "CT Demonstration of the Early Effects of Alcohol on the Brain." In Recent Developments in Alcoholism, 253–64. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-7715-7_20.

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Vetreno, Ryan P., and Fulton T. Crews. "Innate Immune Signaling and Alcoholism." In Neural-Immune Interactions in Brain Function and Alcohol Related Disorders, 251–78. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4729-0_8.

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Nachiappan, V., K. R. Shanmugasundaram, and S. I. Mufti. "Control of Alcoholism by Treatment with SKV, A Herbal Drug Mixture from India." In Alcohol, Cell Membranes, and Signal Transduction in Brain, 185–93. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2470-0_17.

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Conference papers on the topic "Brain Alcoholism Alcohol"

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Prabhakar, Sunil Kumar, Harikumar Rajaguru, and Seong-Whan Lee. "A Comprehensive Analysis of Alcoholic EEG Signals with Detrend Fluctuation Analysis and Post Classifiers." In 2019 7th International Winter Conference on Brain-Computer Interface (BCI). IEEE, 2019. http://dx.doi.org/10.1109/iww-bci.2019.8737328.

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Adhikari, Prakash, Pradeep K. Shukla, Radhakrishna Rao, and Prabhakar Pradhan. "Photonics probing of probiotics effect on chronic alcoholic brain cell nuclei using light localization via confocal imaging." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/cleo_at.2021.am3c.7.

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Adhikari, Prakash, Pradeep K. Shukla, Radhakrishna Rao, and Prabhakar Pradhan. "Quantification of light localization properties to study the effect of probiotic on chronic alcoholic brain cells via confocal imaging." In Imaging, Manipulation, and Analysis of Biomolecules, Cells, and Tissues XIX, edited by James F. Leary, Attila Tarnok, and Irene Georgakoudi. SPIE, 2021. http://dx.doi.org/10.1117/12.2578785.

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