Attention conservation notice: Someone has probably made this point before.
Progeria is a genetic disorder caused by mutations in the lamin A nuclear lamina protein. Since it manifests in several ways that resemble an aged state (eg wrinkled skin, atherosclerosis, kidney failure, loss of eyesight), it is widely believed to be an early-onset version of aging.
Yet, few people think that nuclear membranes are the only thing that is altered in aging, as aging is generally considered too complicated for that. Instead, nuclear membranes are recognized to be one aspect within a larger pathway that is altered in aging.
Familial Alzheimer’s disease (AD) is a genetic disorder caused by mutations in APP, PSEN1, or PSEN2, which are all part of the APP processing pathway and thus (among other things) amyloid plaque production. Since it manifests in several ways that resemble sporadic AD (episodic memory loss, Aβ plaques, tau tangles), it is widely believed to be a an early-onset version of sporadic AD.
In contrast to progeria and aging, familial AD is generally thought to be a model of sporadic AD that captures almost all of the key pathways involved. As a result, one of the major justifications for clinical trials to treat sporadic AD by removing amyloid plaques is that the genetics of familial AD are all related to APP processing and thus amyloid plaque production.
There are probably several good arguments for why this progeria:aging::familial AD:sporadic AD contrast doesn’t make sense, but I still thought it might be interesting.