Background
People with Parkinson’s experience a range of symptoms from physical tremors and slow movements, to sleep disturbances and memory decline (typically associated with dementia). Everyone’s experience of Parkinson’s disease (PD) is different, with symptoms appearing at different ages and progressing at different speeds. Although some cases are genetic (they run in the family), the underlying cause of most cases is unknown.
Why is the study important?
Researchers are still uncovering the causes of PD, and this study has found a potential link between genes and the development of memory problems experienced by some people with PD. This could help us to better understand the causes of PD and to predict disease progression, allowing more personalised treatment plans.
What did the authors do and how did they do it?
In this study, 368 people with PD undertook a variety of tests once a year for 5 years. These tests used a number of techniques to assess things like their memory, language skills and attention, which can reveal the progression of dementia. Participants also underwent a process called genotyping. This allowed researchers to look at their DNA; this is like the body’s instruction manual which we inherit from our parents. Differences in our DNA mean that some people are more at risk of developing certain diseases. In this study, researchers were only interested in one section of DNA, also known as a gene, and this gene is called TOMM40. Everybody’s DNA is different, one of the ways it can differ is by how short or long the instructions for a gene are, and this can affect how well that gene works. In this study, researchers were able to group participants into those with short, long, or very long TOMM40 genes.
What are the results?
Over 5 years, researchers found a decrease in some of the test scores across the whole group, but they saw a larger decrease in those with a short TOMM40 gene. This means that people with a short TOMM40 gene didn’t do as well on the tests than those with a long TOMM40 gene. Splitting participants into those with or without PD dementia, revealed that females with a long TOMM40 gene were less likely to have PD dementia, and that progression to dementia was faster in females with a short TOMM40 gene. Interestingly, this effect was not seen in males, with no association between TOMM40 length and progression to PD dementia.
What do the findings mean going forward for people with the disease?
This study suggests that differences in the TOMM40 gene might be associated with memory decline in people with Parkinson’s, and that these differences could provide protection against dementia in females. The authors suggest that their findings need to be confirmed in a broader and more representative group of people with PD, but that these results could help us to better understand the causes of PD. They may also help to predict disease progression, which could allow us to better tailor treatments to individuals.