A Golgi Study of Cerebellar Atrophy in Human Chronic Alcoholism

Ferrer, Isidre; Fabregues, I.; Pineda, Merçè; Gracia, I.; Ribalta, Teresa

doi:10.1111/j.1365-2990.1984.tb00357.x

Cited by 54 publications

(15 citation statements)

References 12 publications

(5 reference statements)

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“…The cerebellum, known for its importance in motor function, is now additionally thought to play a role in memory disturbance 17. A number of neuropathological studies have established cerebellar atrophy in chronic alcohol abuse 18. Mammillary body atrophy is almost universal in chronic alcoholism.…”

Section: Resultsmentioning

confidence: 99%

Effects of drinking on late-life brain and cognition

Topiwala

Ebmeier

2017

Evid Based Mental Health

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Alcohol consumption is common in Western countries and has been increasing in older adults. Latest figures from Great Britain suggest 75% of those over 65 years drink, an increase from 71% 10 years ago. Chronic heavy intake is a well-established cause of brain atrophy and dementia, with a recent long-term prospective study from the USA reporting a doubling of the odds of later severe memory impairment in those with a history of an alcohol use disorder. Drinking of moderate amounts has been reported to be protective for brain health in a number of epidemiological studies, including some claims of possibly reducing dementia risk. Rigorous recent research has questioned this belief, with new evidence of harmful associations in moderate drinkers compared with abstainers. This has raised suspicion that reported protective effects of moderate drinking were due to confounding by socioeconomic class and intelligence. Clinicians should look out for cognitive impairment in heavy drinkers, considering that abstinence may induce a degree of clinical improvement. Discussions with patients regarding moderate drinking should be informed by recent research. Health benefits of moderate drinking at least for cognitive function are questionable, and if they exist are probably limited to one unit of alcohol daily with respect to other body systems. IntroduCtIonAlcohol use is widespread and increasing across the developed world. Latest figures suggest that 58% of the UK population is drinking in excess of existing safe limits, 1 with 5% men and 4% of women consuming hazardous amounts (>50 units (400 g) for men and >35 units (280 g) for women weekly). Drinking in women and older adults of both sexes has been increasing, 2 with the percentage of those >65 years drinking increasing from 71% to 75% between 2005 and 2016. Those over 65 years of age are now more likely than any other age group to have drunk on at least 5 days in the preceding week.1 Alcohol-related harm is estimated to cost England around £21 billion per year, with £3.5 billion to the NHS, £11 billion tackling alcohol-related crime and £7.3 billion from lost work days and productivity costs. Health concerns associated with alcohol use have focused on liver dysfunction and more recently cancer. The public are largely ignorant of the potential risks of drinking with regards to cognition, in contrast to widespread knowledge of effects on the liver.3 Recommended drinking guidelines have remained unchanged in the UK from 1987 until 2016. Safe limits for men were set at 21 units (168 g) and for women at 14 units (112 g) per week pre-2016. Recent evidence of associations with cancer risk 4 at lower doses prompted revision of UK government alcohol guidance to 14 units (112 g) for both sexes, but current US guidelines still suggest that up to 24.5 units (196 g) weekly is safe for men.This clinical review summarises established effects of chronic heavy drinking on brain and behaviour/cognitive function, as well as the poorly understood impact of moderate consumption. Impl...

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Section: Resultsmentioning

confidence: 99%

Effects of drinking on late-life brain and cognition

Topiwala

Ebmeier

2017

Evid Based Mental Health

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“…Cortical morphology varies with age and with the pathological state of the patient (Kitagaki et al 1998;Symonds et al 1999;Resnick et al 2000;Narr et al 2001a,b;Tang et al 2001;Hardy and Selkoe 2002). Reductions in the volume of specific brain regions occur in certain diseases; they are particularly evident in Alzheimer's disease (Anderson and Hubbard 1981;Ulrich and Stahelin 1984;Najlerahim and Bowen 1988;Tanabe et al 1997;Salat et al 1999;Regeur 2000), alcoholism Kril 1985, 1986;Pfefferbaum et al 1997Pfefferbaum et al , 2001Hommer et al 2001) and alcoholic cerebellar degeneration (Ferrer et al 1984;Kril and Butterworth 1997) and may also occur in schizophrenia (Brown et al 1986;Nasrallah 1995;Lauriello et al 1997;Sullivan et al 1998;De Lisi 1999;Hulshoff-Pol et al 2002). Alterations in the relative proportions of neurones and glial cells can arise from altered brain pathology and can contribute to altered functional characteristics (Benes et al 1987).…”

Section: Tissue Dissectionmentioning

confidence: 99%

Biochemical and molecular studies using human autopsy brain tissue

Hynd

Lewohl

Scott

et al. 2003

Journal of Neurochemistry

221

171

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The use of human brain tissue obtained at autopsy for neurochemical, pharmacological and physiological analyses is reviewed. RNA and protein samples have been found suitable for expression profiling by techniques that include RT-PCR, cDNA microarrays, western blotting, immunohistochemistry and proteomics. The rapid development of molecular biological techniques has increased the impetus for this work to be applied to studies of brain disease. It has been shown that most nucleic acids and proteins are reasonably stable postmortem. However, their abundance and integrity can exhibit marked intra-and intercase variability, making comparisons between case-groups difficult. Variability can reveal important functional and biochemical information. The correct interpretation of neurochemical data must take into account such factors as age, gender, ethnicity, medicative history, immediate ante-mortem status, agonal state and post-mortem and post-autopsy intervals. Here we consider issues associated with the sampling of DNA, RNA and proteins using human autopsy brain tissue in relation to various ante-and postmortem factors. We conclude that valid and practical measures of a variety of parameters may be made in human brain tissue, provided that specific factors are controlled.

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“…Chronic alcoholism results in global brain atrophy with typical points of predilection for neurotoxic effects (16). Alcohol can also induce cortical and subcortical cerebral atrophy (15,16), atrophic changes in the cerebellum (17), enlargement of the cerebrospinal fluid space (15,18), and hippocampal volume loss (16,(19)(20)(21). Moreover, genetic factors (22), gender (23), age (24), amount of consumed ethanol, and the duration of alcohol consumption (25) may all affect the degree of alcohol-related brain damage.…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

Kim¹,

Jeong²,

Yang³

et al. 2011

BMB Reports

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Chronic alcohol consumption contributes to numerous diseases, including cancers, cardiovascular diseases, and liver cirrhosis. Epidemiological studies have shown that excessive alcohol consumption is a risk factor for dementia. Along this line, Alzheimer's disease (AD) is the most common form of dementia and is caused by the accumulation of amyloid-β (Aβ plaques in neurons. In this study, we hypothesized that chronic ethanol consumption is associated with pathological processing of APP in AD. To investigate the relationship between chronic alcohol consumption and Aβ production, brain samples from rats fed an alcohol liquid diet for 5 weeks were analyzed. We show that the expression levels of APP, BACE1, and immature nicastrin were increased in the cerebellum, hippocampus, and striatum of the alcohol-fed group compared to the control group. Total nicastrin and PS1 levels were induced in the hippocampus of alcohol-fed rats. These data suggest that the altered expression of APP and Aβ-producing enzymes possibly contributes to the chronic alcohol consumption-mediated pathogenesis of AD. [BMB reports 2011; 44(2): 135-139]

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A Golgi Study of Cerebellar Atrophy in Human Chronic Alcoholism

Cited by 54 publications

References 12 publications

Effects of drinking on late-life brain and cognition

Effects of drinking on late-life brain and cognition

Biochemical and molecular studies using human autopsy brain tissue

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

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