Progeria is caused by a mutation in Lamin A (LMNA), a gene that codes for a vital component of cellular structure. The cells of progeria patients are misshaped and dysfunctional, leading to symptoms that appear superficially similar to highly accelerated aging. One of the outcomes of this discovery is a broadening of research into lamin proteins in normal aging; researchers have found low levels of malformed lamins and related proteins in older individuals. Evidence is accumulating for the presence of these proteins to contribute to aspects of aging, but the size of the effect is still very much in question. It may or may not be significant in comparison to, say, the harms caused by the various forms of molecular damage outlined in the SENS rejuvenation research programs. The open access paper here delves into an association between lamins and muscle cells, drawing a potential connection to the loss of muscle mass and strength that occurs with age, a condition called sarcopenia.
Biological aging involves complex dysfunctional cellular processes with unclear underlying mechanisms, including a potential involvement of alterations at the nuclear level in a wide range of tissues. Normal nuclear function requires lamin
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