Alcoholism shares a robust relationship with dementia risk, and the correlative literature is getting stronger by the decade.
As of 2020, Alcohol-related brain damage (ARBD) is studied to affect roughly one in 200 members of the general adult population.
Young adults are disproportionately represented among this demographic for various reasons.
If no major interventions take place, health systems project the number of ARBD cases to reach 152 million worldwide by 2050.
New data published by researchers at the Feinstein Institute for Medical Research in New York, suggests that Alzheimer’s disease specifically induced by binge drinking may appear earlier than it does in patients genetically predisposed to develop the condition.
The compounds in alcoholic beverages are uniquely corrosive to the molecular mechanisms that shield us from cognitive decline.
Ladders has covered these mechanisms many times in the past–namely in relation to a protein called tau. When produced in excess, the protein facilitates the build-up of plaques, tangles, and beta-amyloid protein deposits linked with AD.
Beta-amyloid deposits have been actually been independently linked to binge drinking in the past.
“Early-stage studies suggest that alcohol aggravates beta amyloid deposition by increasing the levels of amyloid precursor protein (APP), which increases the enzyme that changes the precursor into beta amyloid and decreases the cellular disposal of beta amyloid. We have decided to focus our research on the effects of alcohol on tau, however, because tau deposition correlates better with the cognitive decline in Alzheimer’s disease than beta amyloid,” the researchers explained in a media release.
The process by which a molecule’s neurological role is chemically augmented is called phosphorylation. The authors of the new report believe that excessive alcohol consumption can lead to phosphorylated tau proteins.
From the report:
“Alzheimer’s disease (AD) is the sixth leading cause of death in the USA and the most common form of neurodegenerative dementia. In AD, microtubule-associated protein tau becomes pathologically phosphorylated and aggregated, leading to neurodegeneration and the cognitive deficits that characterize the disease. Prospective studies have shown that frequent and heavy alcohol drinking is linked to early-onset and increased severity of AD.”
Correlative association between binge drinking and Alzheimer’s Disease
“The precise mechanisms of how alcohol leads to AD, however, remain poorly understood. We have shown that extracellular cold-inducible RNA-inding protein (eCIRP) is a critical mediator of memory impairment induced by exposure to binge-drinking levels of alcohol, leading us to reason that eCIRP may be a key player in the relationship between alcohol and AD,” the authors continued. “In this review, we first discuss the mechanisms by which alcohol promotes AD. We then review eCIRP’s role as a critical mediator of acute alcohol intoxication-induced neuroinflammation and cognitive impairment. Next, we explore the potential contribution of eCIRP to the development of alcohol-induced AD by targeting tau phosphorylation. We also consider the effects of eCIRP on neuronal death and neurogenesis linking alcohol with AD. Finally, we highlight the importance of further studying eCIRP as a critical molecular mechanism connecting acute alcohol intoxication, neuroinflammation, and tau phosphorylation in AD along with the potential of therapeutically targeting eCIRP as a new strategy to attenuate alcohol-induced AD.”
Biological hallmarks associate with AD seemed to consistently attend excessive alcohol consumption.
The Dietary Guidelines for Americans defines moderate alcohol consumption as having up to one drink per day for women and up to two drinks per day for men.
Binge drinking denotes a blood alcohol concentration of 0.08 percent – or 0.08 grams of alcohol per deciliter – or higher.
More broadly, this criterion corresponds to consuming five or more drinks (male), or four or more drinks (female), over the course of two hours.
“Studies have shown that frequent and heavy alcohol drinking is linked to earlier onset and increased severity of Alzheimer’s disease,” Dr. Max Brenner, assistant professor at the Feinstein Institutes explained in Medical Xpress. “It has been reported that alcohol consumption correlates with Alzheimer’s-like cortical atrophy in individuals at high risk of developing the disease as well as younger age of onset.
In addition, chronic alcohol exposure caused neural tau phosphorylation in the hippocampus and memory-impairment in Alzheimer’s-predisposed mice,” the researchers added.
The authors intend to conduct more research to determine the exact parameter surrounding AD and binge drinking. Considering the rising reports of alcohol abuse sweeping pandemic American, readers would do well to limit their intake in accordance with health guidelines in the meantime.
“CIRP is normally present in the cell nucleus where it helps to regulate which proteins each cell produces,” Brenner explained. “When cells detect potentially harmful conditions, such as alcohol exposure, they release molecules like eCIRP to alert other cells nearby to start preparing their defenses to overcome the stress conditions. The cells being alerted recognize eCIRP outside the cell when it binds to specific protein receptors in the cell membrane. The cascade of eCIRP proteins is triggered when alcohol diffuses throughout the brain, and while alcohol is a major influence, the eCIRP cascade can occur under other deleterious conditions. A number of potentially harmful conditions trigger the release of eCIRP, including low oxygen, low temperature and radiation exposure,” Brenner said.