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How Does Alcohol Cause Dementia
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Bin Peng Bin Peng Scilit Preprints.org Google Scholar 1, Qiang Yang Qiang Yang Scilit Preprints.org Google Scholar 2, Rachna B Joshi Rachna B Joshi Scilit Preprints.org Google Scholar 1, 3, Yuancai Liu Yuancai Liu Scilit Preprints.org Google Scholar 2, Mohammed Akbar Mohammed Akbar Scilit Preprints.org Google Scholar 4, Byoung-Joon Song Byoung-Joon Song Scilit Preprints.org Google Scholar 5, Shuanhu Zhou Shuanhu Zhou Scilit Preprints.org Google Scholar 6, * and Xin Wang Xin Wang Scilit Preprints .org Google Scholar 1, *
Hubei Provincial Key Research Institute on Quality and Safety of Traditional Chinese Medicine Health Foods, Jing Brand Research Institute, Daye 435100, China
Leisure Time Sedentary Behaviors Are Differentially Associated With All Cause Dementia Regardless Of Engagement In Physical Activity
Department of Neuroscience and Behavior, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA.
Section of Molecular Pharmacology and Toxicology, Membrane Biochemistry and Biophysics Laboratory, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20892, USA.
Received date: February 25, 2020 / Revision date: March 24, 2020 / Acceptance date: March 24, 2020 / Publication date: March 27, 2020
Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) are increasing as populations age around the world. In most cases, environmental factors also play an important role. Alcohol consumption is widespread and serves as one of the environmental factors that promotes these neurodegenerative diseases. The brain is the primary target of alcohol’s effects, and heavy alcohol consumption has long been associated with brain damage. Chronic alcohol consumption causes permanent neuronal damage associated with increased glutamate-induced excitotoxicity, oxidative stress, and malnutrition. The relationship and contributing mechanisms between alcohol and these three diseases are different. Epidemiological studies have reported that the prevalence of Alzheimer’s disease is reduced in people who consume less alcohol. Low or moderate concentrations of ethanol protect hippocampal neurons from β-amyloid (Aβ) toxicity. Excessive amounts of ethanol increase the accumulation of Aβ and tau phosphorylation. It has been suggested that alcohol is either protective or not associated with PD. However, animal studies suggest that chronic heavy alcohol intake may have dopaminergic neurotoxic effects through induction of cytochrome P450 2E1 (CYP2E1) and increased amounts of α-synuclein (αSYN), which is associated with PD. It has been shown that Findings regarding the association between alcohol consumption and ALS are inconsistent. Recent population-based studies suggest that alcohol consumption does not seem to affect her risk of developing ALS. Further research is needed to clarify the potential etiological involvement of alcohol consumption as a cause or consequence of major neurodegenerative diseases, and ultimately It will lead to a cure.
Alcohol And Testosterone: Long Term & Short Term Effects
As the population ages, more attention should be paid to age-related neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) [1] . These neurological diseases are chronic and progressive, reducing the quality of life of both patients and their caregivers and placing a significant economic burden on society [2]. A small number of cases are caused by known genetic mutations, and studying these mutations will help understand the pathogenesis of these neurodegenerative diseases [3]. However, in most cases, environmental factors play an important role, acting as susceptibility factors and/or triggers [4].
Several environmental factors are associated with these neurodegenerative diseases [5, 6, 7]. The main risk factors for AD, PD, and ALS are shown in Table 1. Alcohol consumption is widespread throughout the world. Complex genetic and environmental factors are thought to determine the pathophysiological effects of alcohol use [8]. The relationship between alcohol consumption and various disorders has been studied for decades [9]. Light to moderate regular intake may be beneficial [10]. However, chronic and excessive drinking can lead to changes in the nervous system [11], liver disease [12], cardiotoxicity [13], mental disorders [14], cancer [15], endocrine [16], microbiome [14] ], immune destruction [17].
Chronic alcohol consumption has significant effects on humans through complex mechanisms (Figure 1). Ethanol affects neurotransmitter systems in a variety of ways, playing a detrimental role. Ethanol stimulates inhibitory γ-aminobutyric acid (GABA) receptors and inhibits excitatory glutamate receptors [20]. After drinking, alcohol can cause temporary euphoria, which then progresses to respiratory depression and coma in a dose-dependent manner [21]. Furthermore, chronic alcohol consumption is associated with increased glutamate-induced excitotoxicity, oxidative stress [22], dementia with decreased cognitive and executive function, cerebellar degeneration with decreased motor performance and ataxia, and multiple It causes permanent neurological damage associated with malnutrition, such as neuropathy and Wernicke’s. and Korsakoff syndrome [23]. Ethanol also negatively affects the availability of nerve growth factor and brain-derived neurotrophic factor, causing impairment of intracellular signaling pathways [23]. However, some studies have shown that moderate ethanol intake has neuroprotective effects. Additionally, alcohol can increase insulin sensitivity [24], stimulate fibrinolysis [25], inhibit thrombin activity [26], prevent platelet aggregation [27], and reduce inflammatory markers [ 28].
There is accumulating evidence that alcohol intake alters the microbiome and the microbiota-gut-brain axis [14]. Alcohol-induced changes in the microbiome can cause neuroinflammation and alter the balance of neuroimmune function. On the other hand, excessive amounts of alcohol interact with neurotransmitter systems and increase the permeability of the blood-brain barrier (BBB), leading to brain damage and dysfunction [20]. The gut microbiota plays an important role in the development of neurodegenerative diseases. Recent studies have shown that probiotics may improve the symptoms of neurodegenerative diseases, and there may be a link between gastrointestinal changes and the pathogenesis of many neurological diseases, including AD, PD, and ALS. A relationship has been suggested [29].
What Is Alcohol Dementia And Can It Be Reversed?
Depending on the amount consumed, alcohol plays a dual role in either exacerbating or protecting against neurodegenerative diseases (Figure 2). Epidemiological studies have reported that the prevalence of Alzheimer’s disease is reduced in individuals who consume small amounts of alcohol [30]. Animal and cellular studies have shown that low or moderate concentrations of ethanol attenuate β-amyloid (Aβ)-induced damage in AD [30, 31, 32, 33]. High concentrations of ethanol contribute to increased accumulation/production of Aβ and precursor proteins [34]. A recent study showed that drinking alcohol in a triple transgenic model of Alzheimer’s disease (3xTg-AD) mice induces deficits in cognitive and emotional function compared to wild-type controls and hyperphosphorylation of tau-Ser199/202 in mice. It has been shown to induce pathological changes such as oxidation. Neuronal cell bodies and dorsal hippocampus (CA1) of 3xTg-AD mice 1 month after drinking [35]. It has been suggested that alcohol is protective or not associated with PD [36]. However, laboratory animal studies have shown that chronic heavy alcohol consumption may have dopaminergic neurotoxic effects [37]. Chronic alcohol exposure reduces the levels of dopamine (DA) [38] and increases the amount of α-synuclein (αSYN), which is associated with the development of PD [39]. Findings regarding the association between alcohol consumption and ALS are inconsistent. A recent population-based study suggests that alcohol consumption does not seem to affect her risk of developing ALS [40]. An animal study showed that red wine extract protects cells from glutamate-induced apoptosis and extends the lifespan of transgenic mice expressing human mutant Cu,Zn superoxide dismutase (mSOD1) [ 41]. However, the link between alcohol and ALS has not yet been established.
Although much progress has been made in this area, there are still some uncertain issues that need to be discussed. This article reviews the main neurological effects of alcohol intake on neurological disorders and discusses the epidemiological and experimental relationships between alcohol intake and major neurodegenerative diseases such as AD, PD, and ALS.
As life expectancy continues to increase, the global burden of cognitive impairment and Alzheimer’s disease is increasing. In 2019, approximately 50 million people worldwide were living with dementia, and with one new infection occurring every 3 seconds, the number of people with dementia will increase by 2050. It is expected to triple [43]. Alzheimer’s disease is one of the most common diseases among older adults and is the leading cause of dementia.
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