Multiple Sclerosis Drug Shows Promise for Macular Degeneration
What: Monocytes, a type of white blood cells from patients with AMD have a reduced ability to ingest waste particles, and glatiramer acetate, a drug approved to treat multiple sclerosis, showed promise in reversing this deficit.
Where: Gu B et al, Deficits in Monocyte Function in Age Related Macular Degeneration: A Novel Systemic Change Associated with the Disease, Frontiers in Medicine, 2021.
BrightFocus Connection: This work was partially funded through a Macular Degeneration Research (MDR) grant to Robyn Guymer, MBBS, PhD, a senior co-author of this paper and deputy director of the Centre for Eye Research Australia (CERA). Dr. Guymer received the Carolyn K. McGillivray Memorial Award in 2016 to study the underlying mechanisms by which debris accumulates in the retina in AMD. The other senior co-author on this paper, Erica Fletcher OD, PhD, is also a past recipient of a BrightFocus research grant.
Why It Is Important: As AMD progresses, a large amount of debris known as “pseudodrusen” accumulates in the retina. Pseudodrusen differ from “drusen” – fatty lipid deposits in the retina that signal AMD’s onset – and yet they are also thought to contribute to the disease. Under ideal circumstances, a subset of white blood cells known as monocytes scavenge bacteria and dead cells and remove them through a process called phagocytosis. However, in intermediate and late AMD, monocytes show reduced phagocytosis compared to healthy controls.
In this study, researchers from the University of Melbourne and CERA tested the ability of monocytes from AMD patients to carry out phagocytosis in a laboratory setting. They found that application of the drug glatiramer acetate, which is approved for the treatment of multiple sclerosis, enhanced phagocytosis in monocytes of patients with both intermediate and late AMD.
The researchers monitored the uptake of fluorescent beads, a measure of phagocytosis, across the three monocyte subtypes in blood from healthy controls or from patients with AMD. In both intermediate and late AMD, phagocytosis was reduced by roughly 40% in all three monocyte subtypes, compared to healthy controls. For the two most common subtypes, incubation with glatiramer acetate restored a significant amount of phagocytosis.
Follow-up studies will seek to determine whether the observed reduction in phagocytosis plays a causal role in the development of AMD, perhaps by driving the accumulation of debris. If defective phagocytosis is shown to be a causative factor, then restoring phagocytosis with glatiramer acetate or another drug may prove a valuable treatment approach.