Age-related macular degeneration (AMD) causes loss of central visual function that ultimately leads to blindness. Prominent in older populations, AMD is the number one cause for blindness in the developed world. The decline in central visual function stems from the degeneration of the macula. Early on, the degeneration of the macula is caused by changes in the retinal Bruch's membrane (BM) that served as the basement membrane of the retinal pigment epithelium (RPE) layer. Loss of RPE layer patency leads to mal-nourishment of the photoreceptor layer leading to impairment of visual function.

Currently treatments for AMD can only slow or arrest the disease progression, not restore of visual function. The pathophysiological studies of AMD indicate that a way to restore vision is through transplant of autologous RPE or iris pigment epithelial (IPE) cells. A major impediment to the success of this cell based therapy is the survival and proliferation of RPE cells on aged BM. Herein we present efforts to engineer the surface of BM into a suitable scaffold, i.e. one that would promote cellular attachment, proliferation, differentiation into RPE phenotype and long term survival of transplanted cells. To achieve these goals, we have selected the collagenous layer of the BM known as the inner collagenous zone (ICZ) as a potential surface. In conjunction, the dip-pen nanolithography (DPN) method is proposed for producing specific patterns on the BM surface. Additionally, specific binding to the collagen fibers on the ICZ surface is proposed as a method to immobilize bioactive molecules that would elicit desirable cellular responses. Such biomolecules may include the RGD peptide sequence for cellular attachment and VIP or PACAP peptide sequence for its neurotrophic effects.