Alcohol and Alzheimer’s Disease By Mrs Vera West
Alzheimer’s disease is the most common form of dementia, and accounts for 60-80 percent of dementia cases. Consequently, any risk factors that contribute to this disease need to be closely examined. And, it is bad news for those who like to tip the turps, as the saying goes. Scientists at Wake Forest University School of Medicine showed that even small amounts of alcohol can accelerate brain atrophy and increase the number of amyloid plaques. These toxic proteins produce Alzheimer’s disease. As the effect comes from even a small quantity of alcohol, the best bet is not to drink alcohol at all. I expect though, that in this culture, especially Australian hedonism, this idea will be ignored in favour of the immediate “pleasure” of alcohol consumption, to numb he pain of existence under the present regime.
https://www.sciencedirect.com/science/article/pii/S096999612200359X?via%3Dihub
“Abstract
Epidemiological studies identified alcohol use disorder (AUD) as a risk factor for Alzheimer's disease (AD), yet there is conflicting evidence on how alcohol use promotes AD pathology. In this study, a 10-week moderate two-bottle choice drinking paradigm was used to identify how chronic ethanol exposure alters amyloid-β (Aβ)-related pathology, metabolism, and behavior. Ethanol-exposed APPswe/PSEN1dE9 (APP/PS1) mice showed increased brain atrophy and an increased number of amyloid plaques. Further analysis revealed that ethanol exposure led to a shift in the distribution of plaque size in the cortex and hippocampus. Ethanol-exposed mice developed a greater number of smaller plaques, potentially setting the stage for increased plaque proliferation in later life. Ethanol drinking APP/PS1 mice also exhibited deficits in nest building, a metric of self-care, as well as increased locomotor activity and central zone exploration in an open field test. Ethanol exposure also led to a diurnal shift in feeding behavior which was associated with changes in glucose homeostasis and glucose intolerance. Complementary in vivo microdialysis experiments were used to measure how acute ethanol directly modulates Aβ in the hippocampal interstitial fluid (ISF). Acute ethanol transiently increased hippocampal ISF glucose levels, suggesting that ethanol directly affects cerebral metabolism. Acute ethanol also selectively increased ISF Aβ40, but not ISF Aβ42, levels during withdrawal. Lastly, chronic ethanol drinking increased N-methyl-d-aspartate receptor (NMDAR) and decreased γ-aminobutyric acid type-A receptor (GABAAR) mRNA levels, indicating a potential hyperexcitable shift in the brain's excitatory/inhibitory (E/I) balance. Collectively, these experiments suggest that ethanol may increase Aβ deposition by disrupting metabolism and the brain's E/I balance. Furthermore, this study provides evidence that a moderate drinking paradigm culminates in an interaction between alcohol use and AD-related phenotypes with a potentiation of AD-related pathology, behavioral dysfunction, and metabolic impairment.”
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