مقالات پذیرفته شده در هشتمین کنگره بین المللی زیست پزشکی
Genetic effects on Alzheimer's disease
Genetic effects on Alzheimer's disease
Parastoo Einali,1,*Sayna Hassani,2
1. Faculty of Advanced Sciences, Islamic Azad University 2. Faculty of Advanced Sciences Branch, Islamic Azad University
Introduction: Alzheimer's disease (AD) is a complex neurological condition marked by the accumulation of misfolded proteins in the brain. Unraveling the genetic underpinnings of AD is essential for diagnosing the disease, predicting its progression, and devising targeted treatments. Recent breakthroughs in scientific research have delved into the fields of epigenomics and proteomics, aiming to uncover early indicators of AD and explore potential therapeutic options. This review seeks to explore the genetic landscape of AD, with a specific focus on understanding how genetics influence the development of AD pathology.
Methods: We searched for articles from the following databases: PubMed; World Health Organization (WHO) Library; Science Direct; Google Scholar.
Results: Numerous studies have ventured into the intricate genetics of AD, revealing the pivotal role of genetic factors in shaping disease susceptibility and advancement. Genome-wide association studies (GWAS) have pinpointed several genetic regions associated with an elevated risk of developing AD, including variations within genes like APOE, TREM2, and PSEN1. These genetic variations can influence critical biological processes involved in AD pathogenesis, such as the metabolism of amyloid-beta, phosphorylation of tau proteins, and neuroinflammatory responses.
Moreover, epigenetic modifications, like DNA methylation and histone acetylation, have emerged as key players in regulating gene expression patterns and disrupting molecular pathways implicated in AD. Additionally, changes in non-coding RNA, such as microRNAs, have been linked to AD progression, affecting essential processes like synaptic plasticity, inflammation, and neuronal survival.
Conclusion: The findings underscore the intricate relationship between genetics and the pathology of AD, emphasizing the multifaceted nature of the disease. Genetic variations contribute significantly to an individual's susceptibility to AD, shaping crucial molecular pathways involved in disease onset and progression. Epigenetic modifications further refine the AD phenotype, adding complexity to the disease's underlying mechanisms.
Understanding the genetic foundations of AD holds promise for developing tailored therapeutic interventions targeting specific molecular pathways implicated in disease progression. Additionally, genetic biomarkers may facilitate early diagnosis and risk assessment, enabling timely interventions to slow or halt disease progression.
Nevertheless, further research is imperative to fully grasp how genetic and epigenetic factors contribute to AD pathology. Integrated approaches combining genetics, epigenomics, and proteomics offer exciting prospects for unraveling the complexities of AD and identifying novel therapeutic targets to combat this devastating neurological disorder.