Boozing may contribute to Alzheimer’s disease

Boozing may lead to Alzheimer’s: Alcohol stops the brain from clearing away toxic clumps that lead to the memory-robbing disease, reveals study

  • Large quantities of alcohol could make the brain less able to repair itself 
  • Protein clumps could build up more in drinkers’ brains, leading to Alzheimer’s 
  • Alzheimer’s is the leading cause of dementia, which affects millions worldwide
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Binge drinking could increase the risk of getting Alzheimer’s disease, new research has discovered.

Drinking a lot of alcohol reduces the brain’s ability to repair itself and clear away plaques which build up to cause Alzheimer’s, the leading cause of dementia.

It damages the genes which control housekeeping cells in the brain, scientists say, and the finding adds to other research linking drinking and dementia.

Plaques – clumps of protein – called amyloid beta are known to be a cause of brain degeneration in Alzheimer’s patients.

In a healthy brain the body’s own cells can clear the amyloid beta away but alcohol reduces its ability to do this, according to research from the University of Illinois.

The researchers say the findings raise questions about the consequences of people’s drinking habits.


Researchers say binge or heavy drinking could contribute to the development of Alzheimer’s disease by reducing the brain’s ability to get rid of toxic clumps

Drinking alcohol is common and more than 7.5 million people in the UK show signs of alcohol dependence, according to the UK Addiction Treatment Centres.

Meanwhile 2015 data showed 15 million people in the US are thought to have alcohol use disorder.

But now scientists say binge or heavy drinking damages genes which help clear the rogue proteins that form plaques in the brains of patients.

Plaques destroy brain cells

These plaques destroy nerve cells and trigger memory loss and confusion, say scientists.

They are usually broken down by cells called microglia, which engulf and destroy the proteins in a process called phagocytosis.

Microglia have been described as the brain’s ‘gardeners’ as they weed out infections and damage. 

However, researchers found they do not work as well when cells become inflamed, which can be caused by heavy alcohol consumption.  

In an experiment on rats, researchers in Chicago exposed microglial cells to levels of alcohol which would be found in heavy drinkers or people who had been binge drinking. 

This could explain the link between alcohol and dementia 

Within just an hour they found phagocytosis – the brain’s cleaning process – fell by about 15 per cent. 

HOW TO DETECT ALZHEIMER’S

Alzheimer’s disease is a progressive brain disorder that slowly destroys memory, thinking skills and the ability to perform simple tasks.

It is the cause of 60 percent to 70 percent of cases of dementia.

The majority of people with Alzheimer’s are age 65 and older.

More than five million Americans have Alzheimer’s.

It is unknown what causes Alzheimer’s. Those who have the APOE gene are more likely to develop late-onset Alzheimer’s.

 Signs and symptoms:

  • Difficulty remembering newly learned information
  • Disorientation
  • Mood and behavioral changes
  • Suspicion about family, friends and professional caregivers
  • More serious memory loss
  • Difficulty with speaking, swallowing and walking

Stage of Alzheimer’s:

  • Mild Alzheimer’s (early-stage) – A person may be able to function independently but is having memory lapses
  • Moderate Alzheimer’s (middle-stage) – Typically the longest stage, the person may confuse words, get frustrated or angry, or have sudden behavioral changes
  • Severe Alzheimer’s disease (late-stage) – In the final stage, individuals lose the ability to respond to their environment, carry on a conversation and, eventually, control movement

There is no known cure for Alzheimer’s, but experts suggest physical exercise, social interaction and adding brain boosting omega-3 fats to your diet to prevent or slowdown the onset of symptoms.

Study leader Professor Douglas Feinstein says this is the first time this has been discovered, and it could explain the link between booze and dementia. 

Prof Feinstein said: ‘We didn’t continue the study to see whether phagocytosis was further impaired after longer exposures to alcohol.

‘But it appears these changes in microglial cells could be a contributing factor to the development of Alzheimer’s disease.’

The scientists found a similar effect when cells were affected by inflammation alone, which is the body’s response to infections but is also caused by drinking.

Past dementia research points finger at booze

Alzheimer’s disease is most common in people over 65 and is a growing problem worldwide as people live longer.

It causes the brain to fail as the disease develops, causing confusion, memory loss and difficulty moving or speaking.   

Earlier this year a study of more than a million dementia patients in France found heavy drinking is associated with a three times greater risk of the devastating illness.

In a separate 2012 study by the University of Exeter, over 65s in the US who drink heavily at least twice a month were found to be two-and-a-half times as likely to suffer a severe decline in their mental ability and memory as they aged.

Doctors have linked alcohol consumption to the development of dementia in up to a quarter of the estimated 850,000 people in the UK with the condition.

How the research was done 

Researchers exposed rat microglial cells to alcohol, pro-inflammatory chemicals called cytokines, or both, in the lab for 24 hours.

They then looked at how genes changed under each condition – and the impact of alcohol on the cells’ ability to destroy amyloid beta.

They found that 312 genes changed under the alcohol condition, 3,082 for the pro-inflammatory condition and 3,552 for both. 

Only some of the genes were involved in both phagocytosis and inflammation.

Professor Feinstein said: ‘While these studies were performed in isolated cells, our results suggest that alcohol impedes the ability of mircroglia to keep the brain clear of amyloid beta and may contribute to the development of Alzheimer’s disease.’

The team published their findings in the Journal of Neuroinflammation.   

Professor Feinstein added the findings have ‘important implications for Alzheimer’s disease patients as well as those at risk’ of developing the disease.

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