An Alzheimer’s therapy may work double-duty as an effective treatment for normal tension glaucoma, Japanese researchers reported at last week’s ARVO meeting in Vancouver.
A mutation affecting a gene called optineurin E50K is known to cause normal tension glaucoma by encouraging protein aggregation in retinal ganglion cells that leads to cell death. As this shares some pathophysiological features with Alzheimer’s disease, investigators studied whether a popular drug for Alzheimer’s could reduce the aggregation and provide neuroprotective benefits for retinal ganglion cells.
In the study, retinal ganglion cells were generated from induced pluripotent stem cells from two healthy individuals and three patients with the mutation, then these cells were exposed to donepezil and evaluated.
Investigators reported donepezil reduced optineurin aggregation and other effects on the nerve matrix in a concentration-dependent manner for retinal ganglion cells. It decreased expression of other pathophysiologic mediators (p62 and TBK1) in retinal ganglion cells.
From these results, the authors concluded that the study demonstrated donepezil had a neuroprotective effect and may have a role to play in treating normal tension glaucoma for cases involving optineurin E50K mutation.
|Inagaki S, Funato M, Shinsuke Nakamura S, et al. Donepezil, an anti-Alzheimer’s disease drug has the neuroprotective effect on RGCs derived from familial glaucoma patients’ iPS cells. ARVO 2019. Abstract 626-B0104.|