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Progerin may also play a role in normal human aging, since its production is activated in typical senescent cells. [21] Unlike other "accelerated aging diseases", such as Werner syndrome, Cockayne syndrome, or xeroderma pigmentosum, progeria may not be directly caused by defective DNA repair. These diseases each cause changes in a few specific ...
Werner syndrome patients exhibit growth retardation, short stature, premature graying of hair, alopecia (hair loss), wrinkling, prematurely aged faces with beaked noses, skin atrophy (wasting away) with scleroderma-like lesions, lipodystrophy (loss of fat tissues), abnormal fat deposition leading to thin legs and arms, and severe ulcerations around the Achilles tendon and malleoli (around ankles).
Affected individuals typically grow and develop normally until puberty, when they do not experience the typical adolescent growth spurt. The mean age of diagnosis is twenty-four. [13] The median and mean age of death are 47-48 and 54 years, respectively; [14] the main cause of death is cardiovascular disease or cancer. [3] [13]
Fibrodysplasia ossificans progressiva (/ ˌ f aɪ b r oʊ d ɪ ˈ s p l eɪ ʒ (i) ə ɒ ˈ s ɪ f ɪ k æ n z p r ə ˈ ɡ r ɛ s ɪ v ə /; [1] abbr. FOP), also called Münchmeyer disease or formerly myositis ossificans progressiva, is an extremely rare connective tissue disease in which fibrous connective tissue such as muscle, tendons, and ligaments turn into bone tissue (ossification).
An aging-associated disease (commonly termed age-related disease, ARD) is a disease that is most often seen with increasing frequency with increasing senescence. They are essentially complications of senescence, distinguished from the aging process itself because all adult animals age ( with rare exceptions ) but not all adult animals ...
For 7-year-old Emma, the rage is a symptom of Batten disease, the fatal, rare illness with which she was diagnosed at age 4. “But I have to take the book away.
DNA recovered from the bones of ancient Europeans is shedding light on the genetic origins of the debilitating disease multiple sclerosis. Gene that protected humans 5,000 years ago may be linked ...
mutations in ERCC4 cause symptoms of accelerated aging that affect the neurologic, hepatobiliary, musculoskeletal, and hematopoietic systems, and cause an old, wizened appearance, loss of subcutaneous fat, liver dysfunction, vision and hearing loss, renal insufficiency, muscle wasting, osteopenia, kyphosis and cerebral atrophy [74]