A new antibody, which detects the toxic particles that destroy healthy brain cells in dementia patients, can be used to diagnose and track the disease.
Researchers at Cambridge University have designed a way to recognize these particles – called amyloid beta oligomers – that are a hallmark of Alzheimer’s disease.
Antibody production may lead to the development of new diagnostic treatments to detect and control Alzheimer’s early, authors say.
Toxic particles are hard to see, researchers say, but this new antibody has a greater affinity with a three-order size – making them easier to track.
Cambridge University researchers have devised a way to recognize these particles – called amyloid beta oligomers – that are a hallmark of Alzheimer’s disease
The Cambridge team teamed up with researchers from University College London (UCL) and Lund University in Sweden to create the new detection antibody.
Researchers reported in the Proceedings of the National Academy of Sciences that the antibody is very accurate at detecting and quantifying toxic oligomers.
Study leader Professor Michele Vendruscolo, of Cambridge’s Center for Misfolding Diseases, said this addresses an urgent need for quantitative methods to recognize the elusive oligomers.
He said, “Through our innovative design strategy, we have now discovered antibodies to recognize these toxic particles.”
Dementia is one of the leading causes of death in the UK, costing more than £ 26 billion annually – a figure that is expected to more than double in the next 25 years.
Current annual costs to the global economy are estimated to be close to £ 1 trillion.
Alzheimer’s disease, the most common form of dementia, results in nerve cell death and tissue loss throughout the brain – resulting in memory failure, personality changes, and difficulty performing daily activities.
Abnormal clumps of proteins called oligomers have been identified by scientists as the most likely cause of dementia.
While normally responsible for important cellular processes, these proteins become rogue and kill healthy nerve cells when someone has Alzheimer’s disease.
Proteins need to be closely regulated to function properly, the team said.
When this quality control process fails, the proteins expand incorrectly, triggering a chain reaction that leads to the death of brain cells, the Cambridge researchers said.
Misfolded proteins form abnormal clusters called plaques that build up between brain cells, making them unable to properly signal.
Dying brain cells also contain tangled, twisted strands of proteins that destroy a vital cell transport system, meaning that nutrients and other essentials can no longer move through the cells.
Despite the fact that more than 400 clinical studies of Alzheimer’s disease are underway, no drug has been approved to change the course of the disease.
Dementia is the only condition in the top 10 causes of death in Britain without treatment to prevent, stop or slow its progression.
Professor Vendruscolo said that the idea that these particles are the cause of Alzheimer’s disease is a common view, but it has not been fully validated.
This is “in part because amyloid beta oligomers are so difficult to detect, so there are differing opinions about the cause of Alzheimer’s disease,” he said.
“The discovery of an antibody to accurately target oligomers is therefore an important step in monitoring disease progression, determining its cause, and ultimately controlling it.”
The lack of a successful way to detect oligomers has been a major obstacle that Alzheimer’s research has so far failed to overcome.
Antibody production may lead to the development of new diagnostic treatments for early detection and control of Alzheimer’s
This has hindered the development of any form of effective diagnostic or therapeutic intervention, the team says.
The lead author of the study, Dr. Francesco Aprile, of Cambridge’s Center for Misfolding Diseases, said the proteins are difficult to detect, isolate and study.
“Our method makes it possible to generate antibody molecules that can target oligomers despite their heterogeneity, and we hope this can be an important step towards new diagnostic approaches,” said Aprile.
The scientists were able to design antibodies for antigens that are very challenging, such as those that live only for a very short time.
they targeted specific regions of the proteins to create an antibody three times better at recognizing it than other previous attempts.
This difference is the main feature that allows the antibody to specifically quantify oligomers in both in vitro and in vivo samples, the team said.
The researchers hope that this tool will enable the discovery of better drug candidates and the design of better clinical trials for people affected by the devastating disease.
WHAT IS DEMENTIA? THE MURDER DISEASE OVERFLOWING THE SUFFERING OF THEIR MEMORY
Dementia is an umbrella term used to describe a range of neurological disorders
A GENERAL CARE
Dementia is an umbrella term used to describe a range of progressive neurological disorders (affecting the brain) that affect memory, thinking and behavior.
There are many different types of dementia, of which Alzheimer’s disease is the most common.
Some people may have a combination of dementias.
Regardless of the type of diagnosis, each person will experience their dementia in their own unique way.
Dementia is a global problem, but it is most often seen in wealthier countries, where people are likely to live to old age.
HOW MANY people are affected?
The Alzheimer’s Society reports that there are currently over 850,000 people living with dementia in the UK, of which more than 500,000 with Alzheimer’s disease.
The number of people with dementia in the UK is estimated to increase to over 1 million by 2025.
In the US, it is estimated that there are 5.5 million Alzheimer’s patients. A comparable percentage increase is expected in the coming years.
As a person’s age increases, so does the risk of developing dementia.
Diagnosis rates improve, but many people with dementia are still undiagnosed.
IS THERE A TREATMENT?
Currently, dementia cannot be cured.
But new drugs can slow its progress, and the sooner it is noticed, the more effective treatments are.
Source: Alzheimer’s Society