A new type of dementia: It’s never too LATE

Earlier this month the media was buzzing with excitement about a recent report identifying a ‘new type’ of dementia. The brain disorder is known as LATE (or to use its scientific name, Limbic-predominant age-associated TDP-43 encephalopathy.)

What is LATE?

LATE is described as a separate disease that can mimic the symptoms of Alzheimer’s disease such as memory problems. It is important to understand that symptoms of dementia occur due to damage to cells in part of the brain known as the hippocampus. 

This damage can be caused by different things; most commonly the build-up of toxic sticky proteins, tau and amyloid that is seen in Alzheimer’s disease. In LATE there is a build-up of another toxic protein, called TDP-43. It too can damage the brain cells in the hippocampus which explains why the clinical symptoms of LATE are very similar to those of Alzheimer’s disease. 

Think about it in terms of the common cold, over 200 different viruses can cause cold symptoms - there can also be several different causes of dementia symptoms. Although currently it is almost impossible for clinicians to distinguish between LATE and Alzheimer’s disease, there are some key differences.

LATE seems to affect individuals over the age of 80 years, progresses slower than Alzheimer’s disease and tends to only affect memory.

Our research on LATE

So, for all of this time, the build-up of the protein TDP-43 was hiding amongst us and we never knew about it?

Well, in fact researchers such as myself and my colleagues from Newcastle University, have been researching TDP-43 and its role in dementia for a number of years now.

In 2016, when I was an Alzheimer’s Society-funded research associate, we published research about the prevalence and importance of identifying the build-up of TDP-43 in donated human brain tissue. 

The recent report showed that people with Alzheimer’s disease often have LATE as well.  We have shown through our research that LATE can also be present in people with a diagnosis of dementia with Lewy bodies.  

A research breakthrough

The proteins amyloid and tau have been associated with dementia for decades, but we know much less about TDP-43. After 10 years of collecting information from around the world, we are only now, starting to understand its role in dementia. 

This breakthrough was only made possible by the donation of human brain tissue. Without these truly heroic and kind-hearted donations through Brains for Dementia Research and to various brain banks throughout the UK (and the world) it would not be possible for us scientists to make these essential discoveries. 

What’s next?

Dr James Pickett, Head of Research at Alzheimer’s Society said: 

'This type of research is the first step towards more precise diagnosis and personalised treatment for dementia, much as we’ve started to see in other serious diseases such as breast cancer.

'This evidence may also go some way to help us understand why some recent clinical trials testing treatment for Alzheimer’s disease have failed – participants may have had slightly different brain diseases.

'But, more research into LATE is required to clarify specific symptoms, identify biomarkers, understand risk factors and develop treatments.’

The key goal of the LATE report was to raise awareness of LATE and encourage more research to understand the underlying causes and its impact on public health. This will be vital to bring us a step closer to our ultimate goal of preventative, precise and personalised treatments.