UK DRI Centre at Imperial<\/a>, shares the complex nature of Alzheimer\u2019s disease and why there’s more to it than just our genes.
\n<\/strong><\/p>\n
\nDementia diagnosis rates are dropping for the first time ever. I wish I could tell you that this is due to less people developing dementia, and not because more people are living with it undiagnosed. According to research carried out by Alzheimer\u2019s Society, many people are not being diagnosed due to the misconception that memory loss is a normal part of aging. However, memory loss is often an early sign of dementia, particularly in the most common cause known as Alzheimer\u2019s disease. As a result, the Alzheimer\u2019s Society\u2019s Dementia Action Week, an annual awareness campaign, has made diagnosis their featured theme.<\/p>\n
<\/p>\n
The build up<\/b><\/h2>\n
What\u2019s staggering is that the onset of these symptoms is preceded by changes in the brain that have accumulated for up to 30 years. In the early-onset form of Alzheimer\u2019s disease, these detrimental changes are associated with mutations in single genes. In other words, if you carry certain mutations in one of these genes, you will develop Alzheimer\u2019s disease. Sadly, here, your genes are your destiny. In contrast, the late onset form results from the contributions of multiple genetic and environmental factors. Thanks to large scale genetic studies where researchers have scanned the genomes – an organism’s complete set of genetic information – of individuals with Alzheimer\u2019s disease and those without, we are learning which genetic variations are associated with the disease.<\/p>\n
Beyond genes\u00a0<\/b><\/h2>\n
As any scientist will know, with answers come more questions. So we\u2019ve identified these genetic variations associated with Alzheimer\u2019s disease, but which brain cell types do they influence? At which timepoints in the lifespan do they contribute to disease? To complicate matters further, many of the genetic variations associated with Alhzeimer\u2019s disease don\u2019t directly fall within genes, but in the regions that regulate gene activity. What are the mechanisms by which gene activity is regulated to confer Alzheimer\u2019s disease risk? How do environmental factors influence gene regulatory mechanisms? This complex interplay of genes, regulation of gene activity, and environment, are why your genes aren\u2019t always your destiny; this is what I, and all the brilliant scientists I get to work with, want to better understand.<\/p>\n
I\u2019m in the second year of my PhD at the neurogenomics lab at Imperial\u2019s Dementia Research Institute. Working closely with two group leaders within this research theme has given me the opportunity to work on a variety of exciting projects. From comparing different species\u2019 genomes to understand why the human brain is so at risk for disease, to inferring cell type-specific signatures in Alzheimer\u2019s disease.<\/p>\n
Meet the key players<\/b><\/h2>\n
One way by which gene activity is regulated is through chemical modifications to DNA that don\u2019t change the underlying genetic code – this is known as epigenetics. An example of a well studied epigenetic modification is H3K27ac. The presence of H3K27ac is associated with increased gene activity, and aberrant levels of this epigenetic modification have been linked to disease. However, many of the studies looking at H3K27ac in the brain have not taken into account the different cell types present. As part of my PhD, we developed a computational tool to infer which regions in the genome marked by H3K27ac are specific to one of four major brain cell types: astrocytes, microglia, oligodendrocytes, or neurons. Using our tool and H3K27ac data from the brains of individuals of Alzheimer\u2019s disease, we were able to delineate whether genetic and H3K27ac variation associated with the disease localised to a particular cell type. Whereas Alzheimer\u2019s disease associated H3K27ac pointed to oligodendrocytes, genetic risk was associated with microglia. Now, with collaborators from across the world, we are focusing on the role of individual genetic risk factors in subtypes of microglia.<\/p>\n
The golden era of Alzheimer\u2019s disease research<\/b><\/h2>\n
There is still so much we don\u2019t know, but with the advances in technologies and continuous influx of genetic, epigenetic, and cell type data, we truly are on the brink of a golden era for the study of Alzheimer\u2019s disease and other complex brain disorders. Most importantly, much of this research wouldn\u2019t be possible without the individuals who have or will donate their brains to research – science can\u2019t thank you enough.<\/p>\n
<\/p>\n
Kitty Murphy<\/a> is a second year PhD student at Imperial\u2019s Dementia Research Institute<\/a> working in the neurogenomics lab.
\n<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"For Dementia Action Week, Kitty Murphy, second year PhD student at the UK DRI Centre at Imperial, shares the complex nature of Alzheimer\u2019s disease and why there’s more to it than just our genes. Dementia diagnosis rates are dropping for the first time ever. I wish I could tell you that this is due to […]<\/p>\n","protected":false},"author":1657,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[302804],"tags":[11177,272422,377,625,81],"class_list":["post-3569","post","type-post","status-publish","format-standard","hentry","category-department-of-brain-sciences","tag-dementia","tag-disease-awareness","tag-genetics","tag-phd","tag-research"],"yoast_head":"\n
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<\/p>\n