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Indeed, a decrease in ribosome gene expression has been implicated in age- and AD-related changes (Payão et al., 1998), and a decreased rate of protein synthesis has been reported in aged mitochondria (Hudson et al., 1998).
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The BAG1 gene has been implicated in age-related neurodegenerative diseases, including Alzheimer's disease62,63.
Further analysis can provide insights into the cause of maternal-age induced chromosome missegregation, since defects in cohesion maintenance has been implicated in age-dependent meiotic malfunctions in mammals.
In addition, they have been implicated in aging and neurodegeneration, including AD28,29,30,31.
The mitochondria have also been implicated in aging and the development of diseases such as cancer.
Reduced telomere length, or its accelerated attrition, has been implicated in aging, mortality, and several human diseases, including respiratory diseases.
Telomere uncapping has been implicated in aging and cancer, yet the precise mechanism of uncapping and its relationship to cell cycle remain to be defined.
Furthermore, mitochondria and their metabolism have been implicated in aging and several human diseases, including inherited mitochondrial disorders, cardiac dysfunction, heart failure, neurodegenerative diseases, diabetes, and cancer.
Mitochondrial oxidative stress has been implicated in aging, neurodegenerative diseases, diabetes, stroke, ischemia/reperfusion injury, age-related macular degeneration (AMD) and cancer.
They have been implicated in aging processes and the seven human isoforms, Sirt1 7, are considered therapeutic targets, e.g., for cancer and neurodegenerative disorders.
While about 20 of these genetic changes have been implicated in aging in other animals, the rest of the genes' direct role in life span has not been investigated.
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