The humble roundworm offers hope for dementia sufferers

The humble roundworm may offer clues in the fight against dementia and Huntington’s disease.

Scientists discovered that when the creature is taught to sniff danger, this triggered a defence mechanism that protects its neurons from degeneration.  

Those exposed to a certain odour were shown in experiments to have significantly higher rates of brain cell survival.

The discovery opens the doors to a new, non-pharmaceutical treatment for neurodegenerative diseases such as dementia and Huntington’s, say experts.

These diseases occur when nerve cells in the brain or peripheral nervous system become damaged, lose function over time and ultimately die.

Although treatments may help relieve some of the symptoms, there is currently no way to slow the progression.

Alzheimer’s and Huntington’s disease could be fought by stimulating older people’s senses (stock photo)

Professor Veena Prahlad, of the University of Iowa, said: ‘Theoretically, it should be possible to treat these types of diseases if we can figure out how to stimulate that defence mechanism in people and have it activated more consistently to fix damaged cells.

‘We would need to find the same sensory triggers in humans as we have demonstrated… in worms.’ 

Alzheimer’s disease is the most common form of dementia and affects around 5.5 million people in the US and 850,000 in the UK. 

Around 127,000 people in the UK are believed to have Parkinson’s, which causes tremors, slow movements and muscle rigidity. Worldwide, more than 10 million are believed to be affected. 

Key findings 

Roundworms are among the most abundant animals on Earth. They have only 302 neurons, compared to the billions in humans, making them a good animal to study in neurological disease.

The research, published in the journal Science Signaling, analysed how the creatures reacted to stress after exposing a group to the scent of a lethal bacterium.

Their defences were triggered more quickly and cells had a 17 per cent higher survival rate after 18 hours than those given the odour of a benign bacterium.

Professor Prahlad believes the worms exposed to the deadly bacterium ‘learned’ the smell – and the threat it presents – and stored that memory. 

Dementia involves the accumulation of protein damage in cells that the human central nervous system does not address, for reasons largely unknown.


A drug prescribed for diabetes patients reduces the risk of developing Parkinson’s disease by more than a quarter, a major study found.

Researchers from the University of Bergen in Norway discovered glitazones (GTZs) had a protective effect against the degenerative neurological disease.

GTZs users saw a 28 percent drop in their chances of developing it compared with people on metformin, which is the most common medication for type 2 diabetes.

GTZs – also known as thiazolidinediones – are approved in the US and the UK for the metabolic disorder, but are not the primary treatment.

They are thought to work by helping the body to self-clean damaged or ageing brain cells.

The research team zeroed in on a defence mechanism common to all plants and animals, known as the heat shock response.

This mechanism – activated by changes in temperature, salinity and other stressors – triggers the production of ‘molecular chaperones’, which repair or get rid of damaged proteins that have become toxic to the cell.

In humans, as in the roundworms, a key gene involved in synthesising molecular chaperones is HSF1 (heat shock transcription factor) which prevents protein damage that can lead to neurodegenerative diseases.

The roundworms exposed to the odour of the deadly bacterium, called PA14, activated twice the number of molecular chaperones.

Professor Prahlad added: ‘We show the HSF1 response is not a reaction. The animal turns it on in anticipation, and it does that by learning about the threat in its environment.’

The question is whether a similar trigger can be found in humans to boost the ‘feelgood’ chemical serotonin, a shortage of which can cause Alzheimer’s, and is required to put HSF1 on alert.