GINnCIN hypothesis of brain aging: deciphering the role of somatic genetic instabilities and neural aneuploidy during ontogenyReportar como inadecuado




GINnCIN hypothesis of brain aging: deciphering the role of somatic genetic instabilities and neural aneuploidy during ontogeny - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Molecular Cytogenetics

, 2:23

First Online: 25 November 2009Received: 04 November 2009Accepted: 25 November 2009

Abstract

Genomic instability GIN and chromosome instability CIN are two closely related ways to produce a variety of pathogenic conditions, i.e. cancer, neurodegeneration, chromosomal and genomic diseases. The GIN and CIN manifestation that possesses the most appreciable impact on cell physiology and viability is aneuploidy. The latter has been consistently shown to be associated with aging. Classically, it has been considered that a failure of mitotic machinery leads to aneuploidy acquiring throughout aging in dividing cells. Paradoxically, this model is inapplicable for the human brain, which is composed of post-mitotic cells persisting throughout the lifetime. To solve this paradox, we have focused on mosaic neural aneuploidy, a remarkable biomarker of GIN and CIN in the normal and diseased brain i.e. Alzheimer-s disease and ataxia-telangiectasia. Looking through the available data on genomic variations in the developing and adult human central nervous system, we were able to propose a hypothesis suggesting that neural aneuploidy produced during early brain development plays a crucial role of genetic determinant of aging in the healthy and diseased brain.

Electronic supplementary materialThe online version of this article doi:10.1186-1755-8166-2-23 contains supplementary material, which is available to authorized users.

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Autor: Yuri B Yurov - Svetlana G Vorsanova - Ivan Y Iourov

Fuente: https://link.springer.com/







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