Behaviour changes in dementia pinpointed in brain

Researchers have located the site of shrinkage in the brains of people with frontotemporal dementia that causes disturbing changes in behaviour.

Lead researcher Dr Michael Hornberger says this discovery will improve our ability to diagnose the disease, and paves the way for the development of drugs to combat the disease.

“This research is the gateway for us to identify objectively the behavioural changes in frontotemporal dementia,” he says. “Now we know which brain regions to target with future therapeutic approaches.”

a brain scan of frontotemporal dementiaBrain regions in yellow/red show areas of atrophy implicated in disinhibited behaviour in FTD

Frontotemporal dementia (FTD) is a common cause of dementia in people aged under 65 years. The age of onset is typically in the 50s or 60s but affect people as young as 30.

One of the main symptoms of FTD is a loss of normal inhibitions, which can manifest as inappropriate remarks and embarrassing behaviour in public.

“This behaviour can appear very crass and make people feel uncomfortable,” says Dr Hornberger. “The patient doesn’t realise that their actions are inappropriate, but it’s quite disturbing for the family and often they won’t go out in public any more.”

Until now, it was not known which brain regions are responsible for the loss of inhibition in FTD.

Using magnetic resonance imaging (MRI), Dr Hornberger and colleagues determined that atrophy in a network of three brain regions – the majority in an area known as the orbital frontal cortex, located at the front of the brain above the eyes – corresponds with these behavioural changes. He also found that deterioration in the connections (white matter) between these regions plays a role.

“This type of atrophy is specific to frontotemporal dementia, so we can now use brain imaging as a way of distinguishing between Alzheimer’s disease and FTD,” says Dr Hornberger. “This will help clinicians determine the correct treatment for their patient.”

He says being able to objectively measure this symptom will facilitate the development of therapies for FTD.

“In order to develop a drug, you need to know where the dysfunction is in the brain. Now we have the ability to measure any improvement and determine whether particular drugs are effective,” he says.

In the short term, Dr Hornberger says that being able to better predict the appearance of behaviour changes will be of great help to families caring for people with FTD.

“Very often the family thinks the patient is being difficult, and don’t realise that their brain is malfunctioning. We can show now that if a patient has atrophy in the identified brain network, disinhibited behaviour are very likely to occur,” he says. “This helps the families understand the disease and they are able to adapt to the patient’s behaviour a lot better.”