Low concentrations of ethanol protect against synaptotoxicity induced by Aβ in hippocampal neurons

Muñoz, Gastón; Urrutia, Juan C.; Burgos, Carlos F.; Silva, Viviana; Aguilar, Felipe; Sama, Michelle A.; Yeh, Hermes H.; Opazo, Carlos; Aguayo, Luis G.

doi:10.1016/j.neurobiolaging.2014.10.017

Cited by 32 publications

(26 citation statements)

References 61 publications

(68 reference statements)

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“…The results are similar to another observation that low concentrations of ethanol protect against damage induced by Aβ in primary neuronal cultures [30,31] and cell lines [32]. Moreover, they found that after consuming 6% ethanol for 2 months, the learning and memory abilities in 3xTg-AD mice were improved [30]. In another study [33] employing moderate ethanol preconditioning (20-30 mM for 6 days) of organotypic hippocampal-entorhinal slice cultures, it was shown that ethanol had a protective effect on Aβ-induced damage (i.e., neurotoxicity and apoptosis).…”

Section: Studies In Animal and Cell Culture Modelssupporting

confidence: 91%

“…Bate et al [62] reported that low concentrations of ethanol (0.02-0.08%) partially protect cultured cortical and hippocampal neurons against the Aβ-induced synapse toxicity. The results are similar to another observation that low concentrations of ethanol protect against damage induced by Aβ in primary neuronal cultures [30,31] and cell lines [32]. Moreover, they found that after consuming 6% ethanol for 2 months, the learning and memory abilities in 3xTg-AD mice were improved [30].…”

Section: Studies In Animal and Cell Culture Modelssupporting

confidence: 88%

“…Depending on the amounts of intake, alcohol may have dual roles in worsening or in protecting neurodegenerative diseases ( Figure 2). Epidemiological studies have reported a reduction in the prevalence of AD in individuals who ingest low amounts of alcohol [30]. Animal and cell studies show that low or moderate concentrations of ethanol reduce the damage induced by β-amyloid (Aβ) in AD [30][31][32][33].…”

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

“…Higher concentrations of ethanol contribute to increased accumulation/production of Aβ and the precursor protein [34]. One recent study showed that alcohol drinking in the show that low or moderate concentrations of ethanol reduce the damage induced by β-amyloid (Aβ) in AD [30][31][32][33]. Higher concentrations of ethanol contribute to increased accumulation/production of Aβ and the precursor protein [34].…”

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

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Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Peng

Yang²,

Joshi

et al. 2020

IJMS

103

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Neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), increase as the population ages around the world. Environmental factors also play an important role in most cases. Alcohol consumption exists extensively and it acts as one of the environmental factors that promotes these neurodegenerative diseases. The brain is a major target for the actions of alcohol, and heavy alcohol consumption has long been associated with brain damage. Chronic alcohol intake leads to elevated glutamate-induced excitotoxicity, oxidative stress and permanent neuronal damage associated with malnutrition. The relationship and contributing mechanisms of alcohol with these three diseases are different. Epidemiological studies have reported a reduction in the prevalence of Alzheimer’s disease in individuals who drink low amounts of alcohol; low or moderate concentrations of ethanol protect against β-amyloid (Aβ) toxicity in hippocampal neurons; and excessive amounts of ethanol increase accumulation of Aβ and Tau phosphorylation. Alcohol has been suggested to be either protective of, or not associated with, PD. However, experimental animal studies indicate that chronic heavy alcohol consumption may have dopamine neurotoxic effects through the induction of Cytochrome P450 2E1 (CYP2E1) and an increase in the amount of α-Synuclein (αSYN) relevant to PD. The findings on the association between alcohol consumption and ALS are inconsistent; a recent population-based study suggests that alcohol drinking seems to not influence the risk of developing ALS. Additional research is needed to clarify the potential etiological involvement of alcohol intake in causing or resulting in major neurodegenerative diseases, which will eventually lead to potential therapeutics against these alcoholic neurodegenerative diseases.

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Section: Studies In Animal and Cell Culture Modelssupporting

confidence: 91%

Section: Studies In Animal and Cell Culture Modelssupporting

confidence: 88%

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

See 2 more Smart Citations

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Peng

Yang²,

Joshi

et al. 2020

IJMS

103

View full text Add to dashboard Cite

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“…How the alteration of intracellular Ca 2+ handling in astrocytes is correlated to these social behavioral and cognitive symptoms of alcohol intoxication is not clear. We suggest that acute ethanol exposure not only impairs the function of neurons but also disrupts the regulation of [Ca 2+ ]i by neurotransmitters and neuromodulators in astrocytes of the brain [15,16]. The later may play a significant role in alcoholism.…”

Section: Fig 3 Ethanol (Eoth) Treatment Abolishes Intracellular Ca mentioning

confidence: 87%

Alcohol Abrogates Intracellular Ca2+ Elevation by Angiotensin II and ATP in Cultured Rat Astrocytes

Wu¹,

Wu²,

Wang³

2015

Peptides 2015, Proceedings of the 24th American Peptide Symposium

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Experimental laboratory models as tools for understanding modifiable dementia risk

Sinclair,

Canty,

Ziebell

et al. 2024

Alzheimer's & Dementia

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Experimental laboratory research has an important role to play in dementia prevention. Mechanisms underlying modifiable risk factors for dementia are promising targets for dementia prevention but are difficult to investigate in human populations due to technological constraints and confounds. Therefore, controlled laboratory experiments in models such as transgenic rodents, invertebrates and in vitro cultured cells are increasingly used to investigate dementia risk factors and test strategies which target them to prevent dementia. This review provides an overview of experimental research into 15 established and putative modifiable dementia risk factors: less early‐life education, hearing loss, depression, social isolation, life stress, hypertension, obesity, diabetes, physical inactivity, heavy alcohol use, smoking, air pollution, anesthetic exposure, traumatic brain injury, and disordered sleep. It explores how experimental models have been, and can be, used to address questions about modifiable dementia risk and prevention that cannot readily be addressed in human studies.Highlights Modifiable dementia risk factors are promising targets for dementia prevention. Interrogation of mechanisms underlying dementia risk is difficult in human populations. Studies using diverse experimental models are revealing modifiable dementia risk mechanisms. We review experimental research into 15 modifiable dementia risk factors. Laboratory science can contribute uniquely to dementia prevention.

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Low concentrations of ethanol protect against synaptotoxicity induced by Aβ in hippocampal neurons

Cited by 32 publications

References 61 publications

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Alcohol Abrogates Intracellular Ca2+ Elevation by Angiotensin II and ATP in Cultured Rat Astrocytes

Experimental laboratory models as tools for understanding modifiable dementia risk

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