Literature DB >> 17689877

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

Benjamin R Eskenazi1, Noah S Wilson-Rich, Philip T Starks.   

Abstract

Huntington's disease (HD) is a neurodegenerative disorder that, unlike most autosomal dominant disorders, is not being selected against. One explanation for the maintenance of the mutant HD allele is that it is transparent to natural selection because disease symptoms typically occur subsequent to an individual's peak reproductive years. While true, this observation does not explain the population-level increase in HD. The increase in HD is at least partly the result of enhanced fitness: HD+ individuals have more offspring than unaffected relatives. This phenomenon has previously been explained as the result of elevated promiscuity of HD+ individuals. For this to be true, disease symptoms must be expressed during the otherwise asymptomatic peak reproductive years and promiscuity must increase offspring production; however, neither prediction is supported by data. Instead, new data suggest that the mutant HD allele bestows health benefits on its carriers. HD+ individuals show elevated levels of the tumor suppressor protein p53 and experience significantly less cancer than unaffected siblings. We hypothesize that the mutant HD allele elevates carriers' immune activity and thus HD+ individuals are, on average, healthier than HD- individuals during reproductive years. As health and reproductive output are positively related, data suggest a counterintuitive relationship: health benefits may lead to an increased prevalence of Huntington's disease.

Entities:  

Mesh:

Substances:

Year:  2007        PMID: 17689877     DOI: 10.1016/j.mehy.2007.02.046

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  9 in total

1.  Comment on Eskenazi et al.

Authors:  Roger L Albin
Journal:  Med Hypotheses       Date:  2008-03-10       Impact factor: 1.538

2.  Response to Falush: a role for cis-element polymorphisms in HD.

Authors:  Simon C Warby; Henk Visscher; Stefanie Butland; Christopher E Pearson; Michael R Hayden
Journal:  Am J Hum Genet       Date:  2009-12       Impact factor: 11.025

Review 3.  A Tale of Two Concepts: Harmonizing the Free Radical and Antagonistic Pleiotropy Theories of Aging.

Authors:  Alexey Golubev; Andrew D Hanson; Vadim N Gladyshev
Journal:  Antioxid Redox Signal       Date:  2017-10-17       Impact factor: 8.401

4.  Gene dysregulation in Huntington's disease: REST, microRNAs and beyond.

Authors:  Rory Johnson; Noel J Buckley
Journal:  Neuromolecular Med       Date:  2009-05-21       Impact factor: 3.843

5.  Antagonistic pleiotropy as a widespread mechanism for the maintenance of polymorphic disease alleles.

Authors:  Ashley J R Carter; Andrew Q Nguyen
Journal:  BMC Med Genet       Date:  2011-12-12       Impact factor: 2.103

6.  Antagonistic pleiotropy in mice carrying a CAG repeat expansion in the range causing Huntington's disease.

Authors:  A J Morton; E A Skillings; N I Wood; Z Zheng
Journal:  Sci Rep       Date:  2019-01-10       Impact factor: 4.379

Review 7.  Pleiotropic Effects of mTOR and Autophagy During Development and Aging.

Authors:  Kathrin Schmeisser; J Alex Parker
Journal:  Front Cell Dev Biol       Date:  2019-09-11

Review 8.  Antagonistic Pleiotropy in Human Disease.

Authors:  Sean G Byars; Konstantinos Voskarides
Journal:  J Mol Evol       Date:  2019-12-21       Impact factor: 3.973

9.  Possible Role of the Polyglutamine Elongation in Evolution of Amyloid-Related Evolvability.

Authors:  Makoto Hashimoto; Gilbert Ho; Yoshiki Takamatsu; Ryoko Wada; Shuei Sugama; Takato Takenouchi; Eliezer Masliah; Masaaki Waragai
Journal:  J Huntingtons Dis       Date:  2018
  9 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.