Progeria (more correctly Hutchinson-Gilford progeria syndrome) is a condition in which a protein vital to cell structure, lamin A, is mutated. Cells with abnormal structure due to loss of function in lamin A are dysfunctional in many ways, including being very prone to senescence. Patients rarely live past their teens, and exhibit a range of conditions such as cardiovascular disease that appear similar to the age-related diseases suffered in later life by non-mutated people. Calling progeria accelerated aging is incorrect and a source of confusion, however, as illustrated by a recent commentary on the topic.
Children with progeria have a mutation in the relevant gene; instead of producing lamin A, they produce a defective mutant protein called progerin. The cell tries to build the nuclear lamina out of defective progerin instead of normal lamin A, and as a result the cell nucleus is screwed up and can't maintain a normal shape. So then aging happens? My sources don't seem to have a great explanation of this. The UniProt database says that this "acts to deregulate mitosis and DNA damage signaling, leading to premature cell death and senescence". This paper goes a little further, saying that the screwiness in the nuclear lamina prevents DNA repair proteins from doing their job.
So a unified theory of progeria goes: the lamin mutation causes accumulation of defective protein in the nucleus, preventing DNA repair. This makes people accumulate DNA damage faster, and since DNA damage is a major cause of aging, it makes these people age more quickly. Lornafarnib interferes with the production of the defective progerin protein. All of this suggests lornafarnib shouldn't help prevent normal aging. After all, normal aging is caused by lots of processes including gradual expected accumulation of DNA damage - not just the downstream effects of one weird mutant protein.
...except that in doing this research I kept finding people saying that maybe some of aging is caused by this one weird mutant protein. I don't really get what's going on here. I know that often, as age-related damage degrades DNA, a lot of weird malformed proteins pop up and accumulate. Maybe progerin is one of these proteins and causes some of the problems commonly associated with aging?
Age-related diseases occur due to damage and loss of function. As a result of damage, cells are misbehaving, broken, lost and not replaced, following incorrect programs, and so forth. In normal aging, this is the result of a particular balance of various forms of damage and their consequences: cellular senescence, buildup of resilient metabolic waste, mitochondrial damage and dysfunction, stem cell decline, and so forth. In progeria, a completely different form of damage dominates, with the result that cells are misbehaving, broken, lost and not replaced, and so forth. It is not that different, conceptually, from a slow poisoning that interferes with vital cellular functions, some forms of which can also superficially replicate the effects of aging.
The point here being that any form of damage that leads to widespread cellular dysfunction, that is not so severe as to kill the patient quickly, will likely have among its outcomes something that looks like a range of age-related conditions. That doesn't make it aging, nor does it say anything at all about how to go about addressing aging itself. The best way to approach aging is to periodically repair the cell and tissue damage that causes it. The strategies for that repair depend absolutely on the type of damage being repaired. Treatments for poisoning or progeria will, on balance, have little to no relevance to the strategies needed to effectively treat aging.
In the case of progeria this is slightly complicated by the discovery that there is a little broken lamin A to be found in normal old humans. Present thinking is that this is likely connected to cellular senescence. The numbers of senescent cells rise with age, and are clearly important to aging, but likely not because of lamin A. Alternatively, the creation of broken lamin A is happening at a very low level throughout the body as a result of other forms of damage and dysfunction in cells, and it is thus a downstream effect and not all that relevant. The challenge in much of biochemistry is that absent a way to selectively eliminate one mechanism without affecting all of the others, it is very hard to say which of these mechanisms are actually more or less important to the observed outcome.
Another challenge is that researchers do tend to exaggerate the relevance of the work they are doing in order to assist in the grant writing process, but that is a whole different topic. So of course anyone writing a paper on lamin A in normal aging is going to say, absent proof otherwise, that it looks like this may be relevant to aging, and more research into this mechanism is justified.
Is malformed lamin A at all relevant to normal aging? Setting aside the reasonable guess of "no", one can imagine a study of senolytic drugs to clear senescent cells in normally aged animals or humans, with before and after tests of the level of malformed lamin A in various tissues in the body. That would be informative. An effective gene therapy to deliver functional lamin A would also be informative, but the present state of gene therapy vectors is that it is very challenging to deliver a vector even close to globally in the body at usefully high levels. Near all of it ends up in the liver and lungs, usually. That would likely be beneficial for progeria patients, while not beneficial enough to save their lives, but seems unlikely to tell us much in a normally aged animal or human.