Central visual pathways in glaucoma: evidence for distal mechanisms of neuronal self-repair.
As in other age-related neurodegenerative diseases, progression of neurodegeneration in glaucoma involves early axonopathy. In glaucoma, this is marked by degradation of active transport along retinal ganglion cell (RGC) axons projecting from the retina to the brain. In experimental systems, transport degradation occurs first in the most distal site in the RGC projection, the superior colliculus (SC) of the midbrain. Even as degradation progresses from one retinotopic sector to the next, important structures in the affected sectors persist, including synapses from RGC axon terminals onto SC neurons. This structural persistence is accompanied by focally increased brain-derived neurotrophic factor in hypertrophic SC astrocyte glia and defines a therapeutic window of opportunity. Thus, central brain structures in glaucoma may respond to disease-relevant stress by induction of mechanisms useful for maintaining retinal signals.
Department of Pharmaceutical Sciences (SDC), Northeast Ohio Medical University, Rootstown, Ohio; and The Vanderbilt Eye Institute and Vanderbilt Brain Institute (DJC), Vanderbilt University School of Medicine, Nashville, Tennessee.
Samuel D
SD
Crish
David J
DJ
Calkins
D005901:Glaucoma / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D009474:Neurons / Q000502:physiology*; D020127:Recovery of Function / Q000502:physiology*; D014795:Visual Pathways / Q000503:physiopathology*