Premature aging as a consequence of Mis-construction of tissues and organs during body development

TL;DR

This paper proposes that premature aging in genetic disorders results from mis-construction of tissues and organs during development, linking defective development to aging through the process of Misrepair.

Contribution

It introduces the concept that mis-construction during development causes tissue abnormalities leading to premature aging, unifying genetic syndromes and normal aging mechanisms.

Findings

Abnormal tissue structures are common in premature and normal aging.

Mis-construction during development causes tissue abnormalities.

Misrepair maintains tissue structure but contributes to aging.

Abstract

Hutchinson-Gilford Progeria syndrome, Werner syndrome, and Cockayne syndrome are three genetic disorders, in which the children have premature aging features. To understand the phenomenon of premature aging, the similarity of aging features in these syndromes to that in normal aging is investigated. Although these three syndromes have different genetic backgrounds, all the patients have abnormal structures of tissues/organs like that in normal aging. Therefore, the abnormality in tissue structure is the common point in premature aging and normal aging. This abnormality links also a defective development and a defective repair, the Misrepair. Defective development is a result of Mis-construction of the structure of tissues and organs as consequence of genetic mutations. Aging is a result of Mis-reconstructions, the Misrepairs, for maintaining the structure of tissues/organs. Construction-reconstruction of the structure of an organism is thus the coupling point of development and aging. Mis- construction and Mis-reconstruction (Misrepair) are the essential processes for the development of aging-like feathers. In conclusion, premature aging is a result of Mis- construction of tissues and organs during body development as consequence of genetic disorders.