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Related Concept Videos

Alzheimer's Disease: Overview01:26

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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The broken Alzheimer's disease genome.

Cláudio Gouveia Roque1, Hemali Phatnani2, Ulrich Hengst3

  • 1Center for Genomics of Neurodegenerative Disease, New York Genome Center, New York, NY 10013, USA; The Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

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Summary

Genomic and epigenomic research reveals the complex mechanisms underlying late-onset Alzheimer's disease (AD). Integrating these findings offers new avenues for personalized and predictive AD care, moving beyond traditional pathology.

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Area of Science:

  • Neuroscience
  • Genetics
  • Genomics

Background:

  • Late-onset Alzheimer's disease (AD) presents complex pathobiology, challenging therapeutic and preventative strategies.
  • Classical hallmarks of AD pathology do not fully capture the disease's intricate mechanisms.

Purpose of the Study:

  • To review genetic, epigenomic, and gene expression findings in AD pathogenesis.
  • To explore how integrating these data enhances understanding of AD's multicellular imbalances and heterogeneity.

Main Methods:

  • High-resolution sequencing technologies applied to genomic and epigenomic analyses.
  • Integration of genetic, epigenomic, and gene expression data.
  • Review of current literature on AD pathogenesis.

Main Results:

  • Genomic insights, termed the "broken AD genome," provide quantitative evidence beyond classical AD hallmarks.
  • Advances highlight novel biological pathways implicated in AD.
  • Genomic and epigenomic data are revitalizing drug discovery and improving clinical tools.

Conclusions:

  • Integration of multi-omics data offers a clearer understanding of AD's heterogeneous, multicellular nature.
  • Future AD care holds promise for being more personalized and predictive based on these research milestones.