Pathogenesis of Presbyopia: A New Understanding of an Age-Old Disease

FOR MOST OF HISTORY, PRESBYOPIA has been defined as a “normal” refractive error caused by age, with discussion limited to the loss of near vision beginning in our 40s. Because we have had no effective therapeutic interventions available, presbyopia has been accepted as a natural part of life and treated primarily by changing power at either the cornea or the lens, hallmarked with some type of visual compromise. The reality is that presbyopic solutions have failed to adequately address this large unmet market, frustrating both physicians and industry. This has led to a waning interest in presbyopic treatments and a currently empty space for devices and therapeutics to treat this growing population. Recent developments in pharmacological presbyopia therapeutics have sparked a renewed enthusiasm in the advancement of presbyopia treatments. However, the real etiology of the loss of accommodative function and its impact on the eye as we age – beyond just the loss of near vision – has yet to be addressed. As we enter this exciting new age of presbyopia therapeutics, it is essential to understand the complex pathophysiology of the aging eye, as well as the pathogenesis of biomechanical dysfunction of accommodation. Illuminating these pathogeneses must be achieved to realize an effective approach to this progressive disease, which to a large extent has age-related biomechanical implications.