این رویداد خاتمه یافته است و اطلاعات موجود در این سایت صرفا جنبه آرشیو دارد

:: DR. Mohsen Ghanbari


                                                     

دکتر محسن قنبری در پنجمین کنگره بین المللی و هفدهمین گنگره ملی ژنتیک ایران، به عنوان مهمان با موضوع:
A genetic epidemiology approach towards identifying novel biomarkers, molecular targets
and drug repurposing candidates in non-coding transcriptome.
سخنرانی خواهند کرد.

نگاهی به فعالیت و علاقه مندی های ایشان:
In the last five years, part of my research has been focused on the role of lifestyle factors in altering risk of age-related diseases by modifying
epigenetic regulation of gene expression. I conducted several studies to show how lifestyle factors such as diet, smoking or alcohol consumption influence epigenetic mechanisms like DNA methylation and microRNA expression, which subsequently alter risk of diseases.
An example of my own research with societal impact is a large-scale multi-center research that was conducted to examine the effect of coffee and tea consumption on DNA methylation levels of >450,000 CpGs across the genome in over 16,000 participants from 15 population based studies around the world. This research showed that coffee consumption is associated with differential DNA methylation levels at multiple CpG sites. The study revealed that the coffee-associated CpGs are linked to expression levels of certain genes involved in metabolic diseases, implying that coffee-associated epigenetic alteration could be an underlying mechanism explaining the impact of coffee on liver and cardiovscaular health. The findings of this project were published in Nature Communications and got a broad media attention and coverage (e.g., Forbes magazine, Food&Wine, Health, NewScientist).
Another example of my research with societal impact is my work on identifying new blood biomarkers for early diagnosis and monitoring
progression of Alzheimer’s disease (AD). This research was conducted to study the association of plasma levels of four proteins (total-tau,
NfL, amyloid-β40 and 42) with incident AD in >5,000 participants of the Rotterdam Study, and the rates of change over time of these proteins
during ~14 years follow-up in participants who developed AD compare with their matched healthy controls. The results of this study that demonstrate plasma NfL and amyloid-β42 levels can be used to assess the risk of developing AD in a non-demented population almost 10 years before AD diagnosis and to monitor disease progression in AD patients, were published in Brain, a top journal in the field of Neurology.
 



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