Moderate lifetime alcohol intake in middle-aged and older people who don’t show signs of dementia is associated with lower deposits of amyloid-beta, the protein that forms toxic aggregates in the brain and is thought to be involved in the onset of Alzheimer’s disease, a study from Korea found.
The study, “Association of moderate alcohol intake with in vivo amyloid-beta deposition in human brain: A cross-sectional study,” was published in the journal PLOS Medicine.
Previous research has shown that moderate alcohol intake might be protective against the development of Alzheimer’s disease. Preclinical studies done in mice and cells grown in the lab have revealed that alcohol can confer such protection by attenuating molecular disease-causing mechanisms related to amyloid-beta.
However, whether moderate alcohol intake exerts this protective effect by decreasing the accumulation of amyloid-beta in the brain or through an amyloid-independent mechanism is still not known.
The researchers explored the link between alcohol consumption and Alzheimer’s disease in 414 individuals between the ages of 56 and 90 without dementia or alcohol-related disorders. Of these, 280 had normal cognition, and 134 had mild cognitive impairment, a neurological condition in which individuals experience subtle changes in memory. The mean age of the group was 70.9.
These individuals participated in the ongoing Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer’s Disease.
The team used questionnaires to assess current and lifelong levels of alcohol consumption.
Amyloid-beta deposition was measured using an imaging technique called the Pittsburgh compound B position emission tomography (PiB-PET). Neurodegeneration linked to Alzheimer’s was evaluated using magnetic resonance imaging (MRI) and fluorodeoxyglucose positron emission tomography (FDG PET), an imaging technique that quantifies brain function by measuring glucose (sugar) levels.
The analysis revealed that moderate (one to 13 standard drinks per week, with a standard drink defined as one containing 10 grams of pure alcohol) lifetime alcohol intake was significantly associated with lower levels of amyloid-beta deposition, compared with not drinking. Current alcohol intake did not affect amyloid-beta deposition.
A lifelong alcohol intake of less than one drink per week or more than 14 drinks per week was not related to amyloid-beta positivity.
Researchers did not find a link between neurodegeneration or white matter volume and lifetime or current alcohol intake.
The observations were independent of potential confounders such as mutations in the apolipoprotein E gene — a major genetic risk factor for the development of a late-onset form of Alzheimer’s — sex, or clinical diagnosis. However, age was an important factor, since the protective effect of moderate alcohol intake was more prominent in older individuals (75 and older) than younger ones.
“The present findings from middle- and old-aged individuals with neither dementia nor alcohol-related disorders suggest that moderate lifetime alcohol intake may have some beneficial influence on [Alzheimer’s] by reducing pathological amyloid deposition rather than amyloid-independent neurodegeneration or cerebrovascular injury,” the researchers said.
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