There are some factors to help elucidate the pathogenesis. The main one is age. The vast majority of cases I see occur in older patients. This speaks to a vascular insufficiency etiology of some fashion. Also AION is clearly vasculopathy in nature and produces the same field defects as "regular" glaucoma.
Clearly the loss of vascular perfusion slowly over time( a type of involutional process )can cause the defect which produces the field defects. Add to this the genetic predisposition to have a fragile capillary vascular bed which as we age causes loss of perfusion and you have a workable theory for how glaucoma presents clinically. The tilted disk, the myopic disk may just further stress mechanically the vascular bed at the optic nerve head and lamina. It seems reasonable the loss of vital perfusion slowly can cause a loss of laminar support of the NFL. the connective tissue elements just slowly atrophy and cause the cupping from lack of mechanical support . When we compare this slow loss of perfusion with that experimentally caused by high induced IOP over a short period of time it all seems to make sense. The rapidity of experimentally (or clinically) induced elevated IOP can cause glaucomatous like atrophy that looks very much like but is not 100% like that in low tension slow perfusion pressure reduction glucomatous atrophy.
I believe the majority of damage we see in the mainstream patient population is caused by some form of vascular insult (slow or rapid).This model appears to fit the clinical presentations we see, the treatments and the result of these treatments (mostly lowering IOP), the age of the patients most affected and the possible genetic/inheritance picture we see. I believe newer treatment modalities to boost the blood supply to the optic nerve head and thus slow or stop the atrophy will be forthcoming and be of great help in the treatment of this disease.
Even the loss of the cartilaginous scaffolding/timbers of the scleral optic canal and lamina can be attributed to lack of perfusion.