Senile systemic (or age-related) amyloidosis is a late onset disease that is acquired, not inherited. Amyloid deposits accumulate in the body from normal (wild-type) proteins.
The best known example of senile systemic amyloidosis arises from the buildup of wild-type transthyretin (TTR) in the hearts of the elderly. Unlike familial amyloidosis, there are
no mutations of the TTR gene, but the slowly progressive cardiac disease has similar symptoms. Whether mutant or wild-type, TTR-mediated amyloidosis is thought to be more common than AL amyloidosis, though it often goes undiagnosed. For example, wild-type TTR is found in up to 30% of patients showing clinical “heart failure with preserved ejection fraction.”Other examples of senile amyloidosis include: APro (from prolactin); ACal (from calcitonin); AIAPP (from amylin); and AANF (from atrial natriuretic factor). All are derived from the misfolding of wild-type proteins. Despite its name, this condition has no relationship to senility or dementia.