summary: Even small amounts of alcohol consumption can accelerate brain atrophy and increase the formation of amyloid plaques. The findings reveal that alcohol consumption may accelerate the pathology of Alzheimer’s disease.
sauce: Wake Forest University
Alzheimer’s disease is the most common form of dementia, accounting for 60% to 80% of dementia cases, according to the Alzheimer’s Association. Although current research suggests that alcohol use disorders are risk factors for Alzheimer’s disease, the impact of alcohol use disorders on Alzheimer’s disease pathology is an ongoing area of research.
In a new preclinical study, scientists at the Wake Forest University School of Medicine found that even moderate amounts of alcohol can accelerate brain atrophy, the loss of brain cells, and increase the number of amyloid plaques, accumulations of toxic proteins. showed that there is Alzheimer’s disease.
This research Neurobiology of disease.
Dr. Shannon Macaulay, associate professor of physiology and pharmacology at Wake Forest University School of Medicine, said:
The study was led by Dr. Jeffrey Weiner and Dr. McAuley, professors of physiology and pharmacology at the Wake Forest University School of Medicine through the School of Medicine’s Center for Alzheimer’s Disease Research and Center for Translational Alcohol Research.
Using a mouse model of Alzheimer’s-associated pathology, the researchers used a 10-week chronic drinking approach that mimicked human behavior regarding alcohol consumption and gave mice the choice of drinking water or alcohol. . Next, we investigated how voluntary and moderate consumption of alcohol alters healthy brain function and behavior and pathologies associated with the early stages of Alzheimer’s disease.
Researchers have found that alcohol increases brain atrophy, increases the number of amyloid plaques, including more small plaques, and may increase the growth of amyloid plaques later in life. .
Interestingly, researchers also noted that abrupt withdrawal from alcohol increased levels of amyloid beta, a key component of the amyloid plaques that accumulate in Alzheimer’s disease.
Further analysis showed that chronic alcohol exposure is poorly regulated in brain and peripheral metabolism. This is another way to promote the pathology of Alzheimer’s disease. Macauley has previously shown that elevated blood sugar levels increase amyloid beta and amyloid plaques.
In the current study, researchers found that even moderate drinking can raise blood sugar levels and markers of insulin resistance, increasing the risk of not only Alzheimer’s disease, but other diseases such as type 2 diabetes and cardiovascular disease. I got
The study also found that moderate alcohol use altered anxiety and dementia-related behaviors.
“These preclinical findings suggest that even moderate alcohol consumption can cause brain damage,” said Macauley. “Alcohol consumption may be a modifiable risk factor for Alzheimer’s disease and dementia.”
About this drinking and Alzheimer’s disease research news
author: press office
sauce: Wake Forest University
contact: Press Office – Wake Forest University
image: image is public domain
Original research: open access.
“Ethanol exposure alters Alzheimer’s-related pathology, behavior, and metabolism in APP/PS1 miceBy Stephen M. Day et al. neurobiology sick
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Ethanol exposure alters Alzheimer’s-related pathology, behavior, and metabolism in APP/PS1 mice
Epidemiological studies have identified alcohol use disorder (AUD) as a risk factor for Alzheimer’s disease (AD), but there is conflicting evidence about how alcohol use promotes AD pathology. In this study, we used a 10-week moderate two-bottle-choice drinking paradigm to determine how chronic ethanol exposure alters amyloid-β (Aβ)-related pathology, metabolism, and behavior. identified.
APPswe/PSEN1dE9 (APP/PS1) mice exposed to ethanol showed increased brain atrophy and increased numbers of amyloid plaques. Further analysis revealed that ethanol exposure resulted in changes in the distribution of cortical and hippocampal plaque sizes.
Ethanol-exposed mice developed more small plaques and may have increased plaque proliferation later in life. We also demonstrated increased locomotion in the open field test, exploring the central zone. Ethanol exposure also resulted in diurnal changes in feeding behavior, which were associated with changes in glucose homeostasis and glucose intolerance.
Using complementary in vivo microdialysis experiments, we determined how acute ethanol directly modulates Aβ in hippocampal interstitial fluid (ISF). Acute ethanol transiently increased hippocampal ISF glucose levels, suggesting that ethanol directly affects brain metabolism. Acute ethanol also selectively increased ISF Aβ40 but not ISF Aβ42 levels during withdrawal.
Finally, chronic ethanol drinking increased N.-Methyl-d-aspartate receptors (NMDAR) and γ-aminobutyric acid type A receptor (GABA) reductionaR) mRNA levels. This indicates a potential hyperexcitatory shift in the excitatory/inhibitory (E/I) balance of the brain. Collectively, these experiments suggest that ethanol may increase Aβ deposition by disrupting metabolism and brain E/I balance.
Furthermore, this study provides evidence that a moderate drinking paradigm culminates in the interaction of alcohol use with AD-related phenotypes, enhancing AD-related pathologies, behavioral dysfunction, and metabolic disorders. To do.
