Aging-associated diseases

An aging-associated disease is a disease that is seen with increasing frequency with increasing senescence. Age-associated diseases are to be distinguished from the ageing process itself because all adult animals age, but not all adult animals experience all age-associated diseases. Aging-associated diseases do not refer to age-specific diseases, such as the childhood diseases chicken pox and measles. "Aging-associated disease" is used here to mean "diseases of the elderly". Nor should aging-associated diseases be confused with accelerated aging diseases, all of which are genetic disorders.

Examples of aging-associated diseases are cardiovascular disease, cancer, arthritis, cataract, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases rapidly with aging (increases exponentially with age, in the case of cancer).

Patterns of differences
By age 3 about 30% of rats have had cancer, whereas by age 85 about 30% of humans have had cancer. Humans, dogs and rabbits get Alzheimer's disease, but rodents do not. Elderly rodents typically die of cancer or kidney disease, but not of cardiovascular disease.

In humans, the relative incidence of cancer increases exponentially with age for most cancers, but levels-off or may even decline by age 60-75 (although colon/rectal cancer continues to increase).

Victims of some of the so-called segmental progerias are vulnerable to different sets of diseases. Victims of Werner's syndrome suffer from osteoporosis, cataracts and cardiovascular disease, but not neurodegeneration or Alzheimer's disease. Victim's of Down syndrome suffer type 2 diabetes and Alzheimer's disease, but not high blood pressure, osteoporosis or cataracts. Victims of Bloom syndrome most often die of cancer.

Theories
Aging (senescence) increases vulnerability to age-associated diseases, whereas genetics determines vulnerability or resistance between species and individuals within species. Some age-related changes (like graying hair) are said to be unrelated to an increase in mortality. But some biogerontologists believe that the same underlying changes that cause graying hair also increase mortality in other organ systems and that understanding the incidence of age-associated disease will advance knowledge of the biology of senescence just as knowledge of childhood disease]]s advanced knowledge of human development.