Premature aging

Premature aging of the brain, circulation, heart, joints, skin, digestive tract, and immune system can begin at any time of life. Various factors cause the body to deteriorate, including injuries that do not heal completely, allergies, toxic chemicals, and heavy metals, poor nutrition, excessive radiation sunlight, overwhelming stress, and inactivity.
The DNA damage theory of aging proposes that aging is a consequence of unrepaired DNA damage accumulation. Damage in this context includes chemical reactions that mutate DNA and/or interfere with DNA replication. Although both mitochondrial and nuclear DNA damage can contribute to aging, nuclear DNA is the main subject of this analysis. Nuclear DNA damage can contribute to aging either indirectly (by increasing apoptosis or cellular senescence) or directly (by increasing cell dysfunction).

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OMIM ID NAME PROTEINS TYPE ALIASES ABBREVIATIONS PATHWAY(S) RELATED
218600 Baller-Gerold syndrome RECQL4 (RTS) premature aging, skeletal abnormalities, risk of malignant disease, skin problem, chromosomal instability CRANIOSYNOSTOSIS WITH RADIAL DEFECTS
CRANIOSYNOSTOSIS-RADIAL APLASIA SYNDROME
BGS
216400 Cockayne syndrome, TYPE A ERCC8 (CSA) neurodegenerative disease, mental retardation (MR), premature aging, skeletal abnormalities, sensitivity to radiation, NO CANCER development, eye or vision problem Weber-Cockayne syndrome
Neill-Dingwall Syndrome
CSA nucleotide excision repair (NER)
268400 Rothmund-Thomson syndrome (RTS) RECQL4 (RTS) telangiectasia, premature aging, skeletal abnormalities, risk of malignant disease, skin problem POIKILODERMA ATROPHICANS AND CATARACT RTS
277700 Werner syndrome (WRN) RECQL2 (WRN) premature aging, risk of malignant disease, chromosomal instability, eye or vision problem Werner WRN

Last modification date: July 1, 2011