  Retinitis pigmentosa (RP) is a group of inherited degenerative eye diseases
characterized by mutations in the genetic structure of the photoreceptors that
leads to the premature death of both rod and cone photoreceptors. Defects in
particular genes encoding proteins that are involved in either the
photoreceptor structure, phototransduction cascades, or visual cycle are
expressed in the rods but ultimately affect both types of cells. RP is
"typically" manifested by a steady death of rods followed by a period of
stability in which cones survive initially and then inevitably die too. In some
RP cases, rods and cones die off simultaneously or even cone death precedes rod
death (reverse RP). The mechanisms and factors involved in the development of
the different types of RP are not well understood nor have researchers been
able to provide more than a limited number of short-term therapies. In this
work we trace the progression of RP to complete blindness through each subtype
via bifurcation theory. We show that the evolution of RP from one stage to
another often requires the failure of multiple components. Our results indicate
that a delicate balance between the availability of nutrients and the rates of
shedding and renewal of photoreceptors is needed at every stage of RP to halt
its progression. This work provides a framework for future physiological
investigations potentially leading to long-term targeted multi-facet
interventions and therapies dependent on the particular stage and subtype of RP
under consideration. The results of this mathematical model may also give
insight into the progression of many other degenerative eye diseases involving
genetic mutations or secondary photoreceptor death and potential ways to
circumvent these diseases.
