Researchers might have uncovered a new potential cause of Alzheimer’s disease, offering a promising avenue for innovative treatments.

A team from the University of California, Santa Cruz, has suggested in a recent commentary that the scientific community might have been concentrating on the wrong target in dementia research for years.

Historically, countless studies and clinical trials have aimed at therapies targeting amyloid beta, a protein notorious for forming clusters in the brain that can hinder communication between neurons, a hallmark of Alzheimer’s.

However, the researchers from California propose that another, less familiar peptide related to amyloid beta, might be the true culprit behind the disease.

This protein, referred to as amyloid alpha or P3, is produced simultaneously with amyloid beta and has long been considered benign.

After meticulously analyzing existing studies and conducting three of their own, the team suggests that this protein might actually be harmful to brain cells, capable of forming the same detrimental protein aggregates associated with Alzheimer’s.

Dr Jevgenij Raskatov, the chemist who led the piece, said: ‘The P3 peptide is, most likely, not the innocent bystander it was commonly thought to be.

‘There’s still more research to be done, but this could turn Alzheimer’s research on its head.’

Alzheimer’s is a debilitating disease that gradually robs sufferers of the ability to live independent lives (stock image)

He added: ‘P3 is a distinct aggregating peptide that is itself potentially neurotoxic and may be contributing to Alzheimer’s disease.’

More than 7 million Americans have Alzheimer disease and cases are expected to nearly double in the US in the next 25 years, rising to nearly 13 million by 2050.

The disease is debilitating and gradually robs sufferers of the ability to live independently, speak and recognize familiar faces.

Despite spending billions on clinical trials and new drugs targeting amyloid beta proteins, scientists have had little success in treating the disease.

Many experts are now exploring other theories for its causes, including suggestions that it may be linked to damaged blood vessels or  complications in the liver.

In their commentary published in the journal ChemBioChem, however, the scientists argue that it is still likely that a protein build-up in the brain is behind the disease.

Amyloid beta is formed when a much larger protein, called the amyloid precursor protein, is broken up by the enzymes beta-secretase and then y-secretase.

But this same process also forms the P3 protein as an offshoot.

As well as reviewing dozens of studies, the team has also now published three major manuscripts investigating the protein, which show it is at least as capable as amyloid beta of forming amyloid deposits — and maybe producing them more rapidly.

Rebecca Luna’s (pictured here) early-onset Alzheimer’s symptoms appeared in her late 40s. She would black out mid-conversation, lose her keys and leave the stove before returning to find her kitchen full of smoke

Jana Nelson was 50 when diagnosed with early onset dementia, following severe personality changes and a sharp cognitive decline that left her unable to solve simple math problems or name colors

Despite the work, however, Raskatov said other scientists remained unaware of their advances. 

In his review, he found at least four scientific studies published in reputable journals that cited his own team’s work as evidence that P3 was not toxic, the opposite of what they had found. 

He said: ‘We remain in the dark on how this sort of grand confusion may have come about. Clearly, there is more work ahead of us.’ 

Current treatments targeting amyloid beta have had limited results to date, slowing the disease’s progression but not reversing it.

Raskatov added: ‘Progress has been extremely slow, and the current state of the art in Alzheimer’s therapy leaves much to be desired. We need fundamentally new approaches to the problem.’

The team’s work was reviewed by Dr David Teplow, an emeritus professor of neurology at the University of California, Los Angeles, who said it shifted his understanding.

He said: ‘This re-evaluation has far-reaching consequences for both basic science and clinical research into the causes and treatment of Alzheimer’s disease.’