The researchers say that this knowledge could improve the effectiveness of current treatments.
'Because this gene can be detected before the symptoms of Alzheimer’s start, and because this pre-symptomatic phase is thought to be a critical period for treatments that could delay or prevent the disease, it could be a great target for early treatments,' said Dr Ozioma Okonkwo, researcher at the University of Wisconsin School of Medicine and lead author on the study.
Alzheimer’s disease is a neurodegenerative disorder and the most common form of dementia, contributing 60-80 percent of dementia cases. The most prominent symptom is memory loss, particularly for new information, and changes in behaviour.
The study, published in the journal Neurology, followed 1023 healthy, middle-aged people with a heightened risk of Alzheimer’s disease over 13 years. At the beginning of the study, the researchers used blood samples to identify individuals who carried the BDNF Val66Met allele (also referred to as the Met allele). BDNF (brain-derived neurotrophic factor) is a protein that helps neurons survive, grow and specialise.
The researchers evaluated each participant's memory and cognitive skills on up to five occasions. Participants without the Met allele showed slight decreases in verbal learning and memory, while carriers of the Met allele showed greater decreases.
Of the participants, 140 also underwent a scan to assess beta-amyloid plaques in the brain, a hallmark of Alzheimer’s disease. The researchers found that people who both had beta-amyloid plaques and were carriers of the Met allele mutation displayed the most rapid cognitive decline of all groups.
'When there is no mutation, it is possible the BDNF gene and the protein it produces are better able to be protective, thereby preserving memory and thinking skills,' Dr Okonkwo said. He added that previous studies had shown exercise could increase levels of BDNF.
Although the study was one of the largest of its kind, participants were mostly white and Alzheimer’s disease is known to affect ethnic groups differently.
Almost a third of people taking part in the study were carriers of the gene. Dr Doug Brown, Director of Research and Development at Alzheimer’s Society, said:
'These findings should not be cause for alarm, much more research is needed to see whether the results stand up to scrutiny in larger groups of people. However, insights like these could help us better understand what is happening as our brain ages and help to develop new, more personalised, treatments for people with dementia in the future.'