New 'plaque destroying' light therapy could prevent Alzheimer's disease by blitzing dangerous …


Rogue brain proteins that trigger Alzheimer’s disease could be destroyed using cheap light therapy, according to new research.

An optic probe has been developed by scientists that glows over 100 times more brightly when it identifies the fine fibers, or fibrils, of amyloid beta that kill neurons.

The light then oxidizes the fibers to prevent them from clumping together in patients’ brains, which inhibits memory and makes them confused. 

An estimated five-and-a-half million people in the United States suffer from Alzheimer’s, according to the Alzheimer’s Association. 

Experts say this technique could be an inexpensive way for doctors to halt the disease before it impacts the brain’s memory and cognitive function.  

Researchers developed a probe to detect clumping in the brain that leads to dementia and Alzheimer's disease. This probe uses light therapy to target the clumps in the brain

Researchers developed a probe to detect clumping in the brain that leads to dementia and Alzheimer's disease. This probe uses light therapy to target the clumps in the brain

Researchers developed a probe to detect clumping in the brain that leads to dementia and Alzheimer’s disease. This probe uses light therapy to target the clumps in the brain

Professor Angel Marti, an associate professor of chemistry at Rice University in the Houston, Texas, and his team developed the probe because light ‘is a cheap resource.’  

He said light activation allows his team to have ‘exquisite control’ of oxidation.

Professor Marti said: ‘We imagine it might be possible someday to prevent symptoms of Alzheimer’s by targeting amyloid beta in the same way we treat cholesterol in people now to prevent cardiovascular disease.’ 

ALZHEIMER’S: FAST FACTS 

WHAT IS IT?

Alzheimer’s disease is a progressive, degenerative disease of the brain. 

A build-up of abnormal proteins causes nerve cells to die.

This disrupts the transmitters that carry messages, and causes the brain to shrink.

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
  • Difficulties making a phone call 
  • Difficulties following a TV show

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… 
  • …This can lead to aggressive behavior
  • Eventually lose ability to walk
  • May have problems eating and drinking 
  • The majority will eventually need 24-hour care 

HOW ALZHEIMER’S DIFFERS FROM NORMAL MEMORY LOSS:

With ordinary age-related forgetfulness, you will still remember details associated with the thing they’ve forgotten.

For example, you may forget your neighbor’s name in conversation, but you still know that person is your neighbor.

Alzheimer’s sufferers forget the entire context. 

The clumping together of the amyloid beta is one of the main causes of dementia and Alzheimer’s, but drugs that target it have so far failed.

Build-up of the protein is one of the earliest changes seen in patients’ brains, forming sticky plaques and leading to nerve cell death and memory loss.

The probe pinpoints a specific binding site on the protein that could facilitate better drugs to treat the disease. 

The device, described in the journal Chem, targets the fibrils using a rare metal called rhenium – and glows when hit with ultraviolet light.

But when it binds to the toxic protein it becomes more than 100 times brighter – causing it to oxidize. 

‘While we cannot see the rhenium complex we can find the oxidation, or footprint, it produces on the amyloid peptide,’ Professor Marti said.

‘That oxidation only happens right next to the place where it binds. The real importance of this research is that it allows us to see with a high degree of certainty where molecules can interact with amyloid beta fibrils.’

Alzheimer’s is a degenerative brain disease that affects more than five million people living in the United States.

The symptoms can progress slow or gradual depending on the type of disease. 

As the brain cells die in the brain, it causes memory loss and disorientation.

Previous research has studied the use of medication to target the fibrils in the brain that clump because of the disease.

But these medications have had difficulty targeting areas where the clumps occur.

Professor Marti said this device could help solve that problem.   

‘There’s an interest in finding medications that will quench the deleterious effects of amyloid beta aggregates,’ Professor Marti said. 

‘But to create drugs for these, we first need to know how drugs or molecules in general can bind and interact with these fibrils, and this was not well known. 

‘Now we have a better idea of what the molecule needs to interact with these fibrils.’ 

He said the findings are important for the design of new drugs targeting amyloid beta.

If the resulting oxidation keeps the fibrils from aggregating further into the sticky substance found in the brains of Alzheimer’s patients, it offers hope of an effective treatment.

‘If we can modify complexes so they absorb red light, which is transparent to tissue, we might be able to perform these photochemical modifications in living animals, and maybe someday in humans,’  Professor Marti said. 



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