The quest to unravel the mysteries of dementia has led researchers to a fascinating discovery about a common gene variant that seems to play a significant role in doubling the risk of dementia for men. The study, recently published in Neurology, delves into the implications of variants in the haemochromatosis (HFE) gene on the likelihood of developing dementia.
Professor John Olynyk, affiliated with Curtin Medical School and one of the co-authors of the study, sheds light on the prevalence of this genetic variation. He notes that approximately one in three individuals carry a single copy of the H63D variant, while one in 36 people harbor two copies. Interestingly, having a solitary copy does not appear to impact health or raise the risk of dementia. However, individuals with two copies face more than double the risk of developing dementia – an effect observed specifically in men but not women.
In Professor Olynyk’s own words,
“Having two copies of this gene variant more than doubled the risk of dementia in men.”
This gender-specific predisposition raises intriguing questions about why males are particularly vulnerable to this genetic influence compared to their female counterparts.
While altering the genetic variant itself remains beyond our current capabilities, understanding how it influences brain pathways – ultimately leading to cognitive impairment – could open doors for potential treatments. Professor Olynyk emphasizes the need for further research to delve into why this specific genetic variation appears to heighten dementia risk primarily in males.
Notably, routine testing for HFE gene variants is already standard practice in many Western countries like Australia when assessing individuals for haemochromatosis – a disorder characterized by excessive iron absorption. Professor Olynyk suggests that expanding such testing protocols might be beneficial for men at large.
Moreover, despite iron levels being under scrutiny due to its connection with haemochromatosis, there seems to be no direct correlation between blood iron levels and heightened dementia risk among affected males. This hints at underlying mechanisms possibly involving escalated brain injury due to inflammation and cellular damage within the body.
Adding depth to these findings is Professor Paul Lacaze from Monash University, another co-author involved in this groundbreaking research. He underscores how comprehending why men carrying double H63D variants face elevated risks could pave new paths towards personalized strategies for preventing and managing dementia cases.
With over 400,000 Australians grappling with dementia currently – a third being men – insights gleaned from studies like these hold promise for enhancing outcomes among those susceptible to cognitive decline. Professor Lacaze views this research as a prime example showcasing effective collaboration among various Australian research entities aimed at deciphering progressive diseases and enhancing global health standards.
The study leveraged data from ASPirin in Reducing Events in Elderly (ASPREE) trial conducted on over 19,000 healthy older adults across Australia and USA. While initially exploring low-dose aspirin’s risks versus benefits within this demographic group, ASPREE trial data has since become pivotal in driving numerous research endeavors focused on healthy aging principles.
This collaborative effort involved esteemed institutions such as Curtin University, Monash University, The University of Melbourne along with healthcare facilities like The Royal Children’s Hospital, Murdoch Children’s Research Institute and Fiona Stanley Hospital. Such interdisciplinary teamwork underscores not only the complexity but also collective resolve exhibited by these institutions towards advancing knowledge frontiers related to age-related conditions like dementia.
In conclusion…
Leave feedback about this