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Related Concept Videos

Gene Evolution - Fast or Slow?02:05

Gene Evolution - Fast or Slow?

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The genomes of eukaryotes are punctuated by long stretches of sequence which do not code for proteins or RNAs. Although some of these regions do contain crucial regulatory sequences, the vast majority of this DNA serves no known function. Typically, these regions of the genome are the ones in which the fastest change, in evolutionary terms, is observed, because there is typically little to no selection pressure acting on these regions to preserve their sequences.
In contrast, regions which code...
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Gene Evolution - Fast or Slow?02:05

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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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Alzheimer's Disease: Treatment01:22

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Gene Duplication and Divergence02:37

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The seminal work of Ohno in 1970 popularized the idea of gene duplication and divergence. DNA sequence comparison studies reveal that a large portion of the genes in bacteria, archaebacteria, and eukaryotes was  generated by gene duplication and divergence, indicating its critical role in evolution.
The duplicated copies of the gene are called Paralogs. Paralogs with similar sequences and functions form a gene family. Across several species, a large number of gene families are...
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Genome Size and the Evolution of New Genes03:21

Genome Size and the Evolution of New Genes

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While every living organism has a genome of some kind (be it RNA, or DNA), there is considerable variation in the sizes of these blueprints. One major factor that impacts genome size is whether the organism is prokaryotic or eukaryotic. In prokaryotes, the genome contains little to no non-coding sequence, such that genes are tightly clustered in groups or operons sequentially along the chromosome. Conversely, the genes in eukaryotes are punctuated by long stretches of non-coding sequence.
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Related Experiment Video

Updated: Dec 25, 2025

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
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Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration

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Alzheimer-related genes show accelerated evolution.

Anne Nitsche1, Christian Arnold1,2,3, Uwe Ueberham4

  • 1Bioinformatics Group, Department of Computer Science, University Leipzig, Härtelstraße 16-18, D-04107, Leipzig, Germany.

Molecular Psychiatry
|March 24, 2020
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Alzheimer's disease (AD) genes are evolutionarily old, but their structures change rapidly, especially non-coding genes. This suggests recent human brain evolution contributes to AD, challenging current animal models.

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Area of Science:

  • Evolutionary biology
  • Neurogenetics
  • Genomics

Background:

  • Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in humans but rare in other mammals, suggesting a phylogenetic basis.
  • The evolutionary origins and dynamics of AD-associated genes remain largely unexplored.
  • Understanding the evolutionary aspect of AD is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the evolutionary age and structural dynamics of genes associated with Alzheimer's disease (AD).
  • To determine if AD-associated genes exhibit unique evolutionary patterns compared to the broader genome.
  • To explore the role of non-coding RNAs in AD pathogenesis from an evolutionary perspective.

Main Methods:

  • Established a genome-wide RNA profile of AD-associated genes, including protein-coding and non-coding transcripts.
  • Analyzed the conservation of splice-sites across vertebrates for homologs of AD-associated genes to assess gene structure evolution.
  • Compared evolutionary rates of AD-associated gene structures with the general genome.

Main Results:

  • Nearly all AD-associated genes are evolutionarily ancient, originating no later than non-AD-associated genes.
  • Gene structures of loci with AD-associated expression changes evolve faster than the genome average.
  • Non-coding AD-associated loci show significantly accelerated structural evolution compared to protein-coding loci and the genome.

Conclusions:

  • Accelerated evolution of AD-associated genes suggests rapid functional adaptation, particularly in non-coding elements.
  • Recent adaptive evolution of the human brain may be intrinsically linked to neurodegeneration mechanisms in AD.
  • A paradigm shift is needed in AD research, reconsidering animal models and focusing on the evolutionary trajectory of the human brain.