Experimental stroke drug may also prevent Alzheimer’s by ‘preventing the build-up of toxic proteins in the brain’
- Giving mice the medication 3K3A-APC stopped Alzheimer’s symptoms
- 3K3A-APC is used to reduce bleeding within the brain tissue of stroke patients
- Reduces inflammation, and protects nerve cells and the lining of blood vessels
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An experimental drug used to treat stroke may also prevent Alzheimer’s, research suggests.
A study found giving mice the medication 3K3A-APC protects their brains against the build-up of toxic proteins and inhibits memory loss.
3K3A-APC is already used to reduce bleeding within the brain tissue of stroke patients and trials have demonstrated its safety.
A drug used to treat stroke may also prevent Alzheimer’s, research suggests (stock)
The research was carried out by the University of Southern California and led by Dr Berislav Zlokovic, director of the Zilkha Neurogenetic Institute at the Keck School of Medicine.
Alzheimer’s is the most common form of dementia and affects more than 520,000 people in the UK, according to the Alzheimer’s Society.
The disease has around 5.7million patients in the US, Alzheimer’s Association statistics show.
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3K3A-APC is a genetically modified version of a human blood protein called activated protein C, the researchers explained in the Journal of Experimental Medicine.
Activated protein C reduces inflammation, and protects nerve cells and the cells that line the blood vessels from programmed cell suicide, known as apoptosis.
‘Because of its neuroprotective, vasculoprotective, and anti-inflammatory activities in multiple models of neurological disorders, we investigated whether 3K3A-APC can also protect the brain from the toxic effects of amyloid-β toxin in a mouse model of Alzheimer’s,’ Dr Zlokovic said.
Amyloid-β proteins accumulate in the brains of Alzheimer’s patients, which leads to the progressive loss of nerve cells and reduced blood flow through the vital organ.
When injected into mice that were genetically at-risk of Alzheimer’s, the researchers found 3K3A-APC reduced the accumulation of amyloid-β by up to 50 per cent over four months.
This is compared to the control rodents, who were not given 3K3A-APC and experienced cognitive decline, break down of the blood brain barrier and neuroinflammation – a key feature of Alzheimer’s.
3K3A-APC works by preventing nerve cells from producing the enzyme BACE1, which is required to make amyloid-β.
Although inhibitors of BACE1 have been tested before, this study suggests blocking the enzyme’s production may be an effective approach, particularly in the early stages of Alzheimer’s before amyloid-β permanently damages the brain.
‘Our present data support the idea that 3K3A-APC holds potential as an effective anti-amyloid-β therapy for early stage Alzheimer’s disease in humans,’ Dr Zlokovic said.
3K3A-APC has already shown strong safety in stroke patients in clinical trials, as well as in MS and brain trauma studies.
Speaking of the most recent findings, Dr Sara Imarisio, head of research at Alzheimer’s Research UK, told MailOnline: ‘Having had no new dementia treatments in over 15 years it’s important we continue to look at a number of angles to find a life-changing treatment for people with the condition.
‘Amyloid remains one of the key targets for drug developers, however, this is an early stage research study using a drug that is not yet licensed for use in people who have had a stroke.
‘As with any research in mice we must be careful how we analyse the results and much more work is required before a drug like this could be to be repurposed for use in people with Alzheimer’s or any other neurodegenerative disease.’
WHAT IS ALZHEIMER’S?
Alzheimer’s disease is a progressive, degenerative disease of the brain, in which build-up of abnormal proteins causes nerve cells to die.
This disrupts the transmitters that carry messages, and causes the brain to shrink.
More than 5 million people suffer from the disease in the US, where it is the 6th leading cause of death.
WHAT HAPPENS?
As brain cells die, the functions they provide are lost.
That includes memory, orientation and the ability to think and reason.
The progress of the disease is slow and gradual.
On average, patients live five to seven years after diagnosis, but some may live for ten to 15 years.
EARLY SYMPTOMS:
- Loss of short-term memory
- Disorientation
- Behavioral changes
- Mood swings
- Difficulties dealing with money or making a phone call
LATER SYMPTOMS:
- Severe memory loss, forgetting close family members, familiar objects or places
- Becoming anxious and frustrated over inability to make sense of the world, leading to aggressive behavior
- Eventually lose ability to walk
- May have problems eating
- The majority will eventually need 24-hour care
Source: Alzheimer’s Association
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