Drug used to treat high blood pressure could relieve Alzheimer’s
Drug used to treat high blood pressure could relieve Parkinson’s, Huntington’s and Alzheimer’s by encouraging ‘Pac-Man-like cells to eat away toxic protein build-ups in the brain’
- Felodipine reduced the build-up of proteins in the brains of mice and zebrafish
- Triggered ‘defective cells’ to ‘eat themselves’, with the waste then broken down
- Drug dose required in mice was lower than expected, suggesting it is safe
A drug that is used to treat high blood pressure may relieve Parkinson’s, Huntington’s and Alzheimer’s, research suggests.
A study found felodipine reduced the toxic build-up of proteins in the brains of mice and zebrafish with neurodegenerative diseases.
Felodipine triggered the animals’ ‘defective cells’ to undergo autophagy, when cells ‘eat’ themselves like ‘Pac-Man’, with the leftover waste being broken down.
Autophagy occurs naturally in healthy people but is impaired in those with diseases such as Alzheimer’s.
The drug dose required was also lower than anticipated, prompting the University of Cambridge researchers to be ‘cautiously optimistic’ about their findings.
A drug that is used to treat high blood pressure may relieve Parkinson’s, Huntington’s and Alzheimer’s. It works by triggering’ ‘defective cells’ to undergo autophagy. This occurs when cells ‘eat’ themselves like ‘Pac-Man’ (pictured), with the leftover waste being broken down
The team was led by Professor David Rubinsztein, deputy director of the Cambridge Institute for Medical Research and professor of molecular neurogenetics.
‘This is the first time that we’re aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans,’ he said.
‘As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialled in patients.’
Professor Rubinsztein added: ‘This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice.
‘We need to be cautious, but I would like to say we can be cautiously optimistic.’
Parkinson’s, Huntington’s and dementia are all examples of neurodegenerative diseases.
These occur when neurones – cells that carry signals to and from the brain – lose their function over time and ultimately die.
A common feature of these conditions is misfolded proteins, such as huntingtin in Huntington’s disease and tau in some forms of dementia, the authors wrote in the journal Nature Communications.
A study found felodipine reduced the toxic build-up of proteins in the brains of mice and zebrafish with neurodegenerative diseases (stock)
These proteins accumulate to cause irreversible damage to brain cells. And patients with neurodegenerative diseases are unable to clear these proteins due to their autophagy process being impaired.
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
- Mood and behavioral changes
- Suspicion about family, friends and professional caregivers
- More serious memory loss
- Difficulty with speaking, swallowing and walking
Stages 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.
Neurodegenerative diseases already affect millions of people worldwide. More than five million adults in the US are living with Alzheimer’s and at least 500,000 have Parkinson’s, according to the National Institute of Environmental Health Sciences.
And in the UK, 850,000 people have dementia, with Alzheimer’s being the most common type of the disease, Alzheimer’s Society says. And around 145,500 people are living with Parkinson’s, according to Parkinson’s UK.
Neurodegenerative diseases are set to rise as the global population ages, with effective drugs needed more now than ever, the researchers wrote.
However, no medication successfully induces this ‘Pac-Man’ effect – as described by the researchers – in these patients.
When looking for new drugs, scientists often experiment with existing ones due to them already being known to be safe in humans.
Inspired by past studies that found a link between hypertension drug felodipine and a reduced risk of Parkinson’s, the researchers gave the medication to mice that had been genetically modified to express mutations that cause Huntington’s and Parkinson’s.
Mice were chosen due to their short life span and fast reproductive rate, which enables scientists to quickly investigate the biological impact of a drug.
And aspects of the rodents’ physiology share similar characteristics with humans, such as their nervous system.
The scientists also gave felodipine to zebrafish with a form of dementia.
Results revealed both animals showed reduced signs of their respective diseases following treatment.
Although mice studies typically use doses that are much higher than what is considered safe for humans, the researchers saw even low levels of the drug led to benefits for the rodents with Parkinson’s.
They controlled the concentration of the drug being administered via a small pump beneath the mice’s skin.
Fiona Carragher, chief policy and research officer at Alzheimer’s Society – which partially funded the study – added: ‘With no new treatments for dementia in over 15 years, it’s encouraging to see that re-purposing an existing drug has showed signs of reducing key hallmarks of some types of dementia.
‘However, it’s still early days and more research is needed to fully understand this drug’s potential in tackling the symptoms of the condition and to examine dosage and side effects.’
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