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Exploring the selective vulnerability in Alzheimer disease using tissue specific variant analysis.

S Akila Parvathy Dharshini1, Y-H Taguchi2, M Michael Gromiha3

  • 1Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, Tamilnadu, India.

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Summary

Alzheimer's disease (AD) shows selective brain vulnerability. This study identifies specific genetic variations and altered gene functions in temporal and frontal lobes, revealing glial cell disruption as a key factor in AD's selective neurodegeneration.

Keywords:
Age-related macular degenerationAlzheimer's diseaseAmyotrophic lateral sclerosisEpitranscriptomeReactive oxygen speciesSequence alignment/map

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Selective vulnerability of brain regions is key in neurodegenerative disorders like Alzheimer's disease (AD).
  • Hippocampal neurons in the medial temporal lobe are particularly damaged in AD.
  • Identifying tissue-specific genetic variants is crucial for understanding AD's selective vulnerability.

Purpose of the Study:

  • To identify specific genetic variations and altered gene functions in distinct brain lobes affected by Alzheimer's disease.
  • To investigate the relationship between genetic variations, gene expression, and epitranscriptomic modifications in AD.
  • To elucidate the molecular mechanisms underlying selective neuronal vulnerability in AD.

Main Methods:

  • Alignment of mRNA-seq data with genomic assemblies (HG19/HG38) using sequence alignment tools.
  • Comparison with genome-wide association studies (GWAS) and gene expression quantitative trait loci (eQTL) studies.
  • Analysis of RNA modification databases, variant effect evaluation, and construction of genetic/functional interaction networks.

Main Results:

  • Identified specific variations and altered gene expression in temporal (gliogenesis, intermediate filament organization) and frontal lobes (oxidative phosphorylation, calcium ion homeostasis) of AD brains.
  • Found modifications in protein degradation and apoptotic signaling in other affected brain regions.
  • Distinguished between genetic variants and epitranscriptomic modifications, evaluating their effects on coding/UTR regions.

Conclusions:

  • Disruption of glial cell structural integrity, defective gliogenesis, and impaired glia-neuron communication are proposed as primary drivers of selective vulnerability in Alzheimer's disease.
  • Altered pathways in different brain lobes contribute to the complex pathology of AD.
  • Understanding these molecular and cellular changes is essential for developing targeted AD therapies.