A Darwinian approach to Huntington's disease: subtle health benefits of a neurological disorder.

@article{Eskenazi2007ADA,
  title={A Darwinian approach to Huntington's disease: subtle health benefits of a neurological disorder.},
  author={Benjamin R Eskenazi and Noah Wilson-Rich and Philip T B Starks},
  journal={Medical hypotheses},
  year={2007},
  volume={69 6},
  pages={
          1183-9
        }
}
Antagonistic pleiotropy in mice carrying a CAG repeat expansion in the range causing Huntington’s disease
TLDR
This novel mouse line provides direct experimental evidence that, although the HD mutation causes a fatal neurodegenerative disorder, there may be premorbid benefits of carrying the mutation.
Genetic counseling and testing for Huntington's disease: A historical review
  • M. Nance
  • Medicine
    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
  • 2017
TLDR
How the emergence of Huntington's disease registries and patient support organizations, genetic testing, and the discovery of a disease‐causing CAG repeat expansion changed the contours of genetic counseling for families with HD are reviewed.
Comment on Eskenazi et al.
  • R. Albin
  • Medicine, Biology
    Medical hypotheses
  • 2008
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The predictions of two evolutionary explanations of senescence—mutation accumulation and antagonistic pleiotropy—which postulate that genetic variants with harmful effects in old ages can be tolerated, or even favoured, by natural selection at early ages are tested.
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The objective of this paper is to determine whether evolvability could also be applied to the physiological functions of epolyQ, which is widely expressed from microorganisms to human brain, whereas APs are only identified in vertebrates.
3-Nitropropionic Acid as a Tool to Study the Mechanisms Involved in Huntington’s Disease: Past, Present and Future
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This review will focus on the past and present research of 3-Nitropropionic acid, to finally bring a perspective on what will be next in this promising field of study.
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Several features of the expansion mutation in HD are similar to those previously observed for mutations of similar size in spinobulbar muscular atrophy and in myotonic dystrophy, and to those observed more recently in spinocerebellar ataxia type 1 and in dentatorubropallidoluysian atrophy, four diseases also caused by expansion of CAG repeats.
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