Worms reveal link between dementia gene and ageing

July 23, 2013, Science in Public

The discovery of a link between a specific gene and ageing in a species of worm could reveal valuable lessons for the treatment of Alzheimer's disease.

Low levels of the protein generated from the gene known as 'tau'—also present in humans—not only hastens -related changes in the brain of the worm, but also shortens the worm's life, Sydney University PhD candidate Yee Lian Chew has found.

"We found that lacking tau lived almost one third shorter than worms that have tau, providing startling evidence that the gene is important in regulating overall lifespan," said Yee Lian.

Her findings – together with related experiments on mice and other models – could be very important for future Alzheimer's Disease treatments.

"One theory of suggests that lowering the activity of this gene in a patient will lead to some degree of cognitive improvement," she said. "However, too little is also bad. It needs to be a balance."

Yee Lian's work at the university's School of Molecular Bioscience uses a species of nematode worm called Caenorhabditis elegans, which is see-through and just one millimetre long.

The worms are an exceptional way to study brain ageing, she says, as their transparency allows her to easily examine the changes that emerge in older brain cells and to study how fast the brain ages.

"Humans are certainly more complex than worms, but at a molecular level there are many striking similarities," Yee Lian says. "The lack of complexity is also an advantage – worms have 302 brain cells whereas humans have billions. It is much simpler to study brain ageing in an animal where individual cells can be easily observed."

In humans, aging is associated with subtle changes in the . These changes are comparable to those observed in worm brains, such as the growth of structures called branches and beads along fibres known as axons.

"Our most exciting discovery is that worms lacking tau display these abnormal structures at early and middle age, while normal worms that have tau only show these structures late in life," said Ms Chew.

"This suggests that the lack of causes worm to age faster."

The discovery, which was published in the Journal of Cell Science, may lead to valuable clues for the treatment of Alzheimer's Disease, a devastating condition which affects one in four people over the age of 85.

"Our research provides an important stepping stone towards the ultimate goal of improving diagnostic tools and treatments for those suffering from this condition," she said.

Ms Chew is one of 12 early-career scientists unveiling their research to the public for the first time thanks to Fresh Science, a national program sponsored by the Australian Government through the Inspiring Australia initiative.

Explore further: Worming our way to new treatments for Alzheimer's disease

Related Stories

Worming our way to new treatments for Alzheimer's disease

March 7, 2013
According to a 2012 World Health Organization report, over 35 million people worldwide currently have dementia, a number that is expected to double by 2030 (66 million) and triple by 2050 (115 million). Alzheimer's disease, ...

New Alzheimer's research suggests possible cause: The interaction of proteins in the brain

June 19, 2013
For years, Alzheimer's researchers have focused on two proteins that accumulate in the brains of people with Alzheimer's and may contribute to the disease: plaques made up of the protein amyloid-beta, and tangles of another ...

New hope for treating Alzheimer's Disease: A role for the FKBP52 protein

March 20, 2012
New research in humans published today reveals that the so-called FKBP52 protein may prevent the Tau protein from turning pathogenic. This may prove significant for the development of new Alzheimer's drugs and for detecting ...

From trauma to tau: Researchers tie brain injury to toxic form of protein

May 29, 2013
University of Texas Medical Branch at Galveston researchers have uncovered what may be a key molecular mechanism behind the lasting damage done by traumatic brain injury.

Scientists detail alzheimer's progression, step by step

July 16, 2013
(HealthDay)—New research seeks to delineate just how Alzheimer's disease unfolds in the human brain.

Recommended for you

Rocky start for Alzheimer's drug research in 2018

January 19, 2018
The year 2018, barely underway, has already dealt a series of disheartening blows to the quest for an Alzheimer's cure.

Alzheimer's disease: Neuronal loss very limited

January 17, 2018
Frequently encountered in the elderly, Alzheimer's is considered a neurodegenerative disease, which means that it is accompanied by a significant, progressive loss of neurons and their nerve endings, or synapses. A joint ...

Anxiety: An early indicator of Alzheimer's disease?

January 12, 2018
A new study suggests an association between elevated amyloid beta levels and the worsening of anxiety symptoms. The findings support the hypothesis that neuropsychiatric symptoms could represent the early manifestation of ...

One of the most promising drugs for Alzheimer's disease fails in clinical trials

January 11, 2018
To the roughly 400 clinical trials that have tested some experimental treatment for Alzheimer's disease and come up short, we can now add three more.

Different disease types associated with distinct amyloid-beta prion strains found in Alzheimer's patients

January 9, 2018
An international team of researchers has found different disease type associations with distinct amyloid-beta prion strains in the brains of dead Alzheimer's patients. In their paper published in Proceedings of the National ...

Advances in brain imaging settle debate over spread of key protein in Alzheimer's

January 5, 2018
Recent advances in brain imaging have enabled scientists to show for the first time that a key protein which causes nerve cell death spreads throughout the brain in Alzheimer's disease - and hence that blocking its spread ...


Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.