Abstract
Irreversible damage to the structure of axons and death of the retinal ganglion cell (RGC) soma in primary open-angle glaucoma (POAG) and Alzheimer’s disease (AD) develop against the background of the already existing clinical manifestation, which is preceded by a slow period of progressive loss of synapses and dendrites of the RGCs. Recent studies have shown that the integrity of the RGC’s dendritic branching can serve as both a target of neuroprotective therapy and a sensitive marker of retinal degeneration in AD and glaucoma. To develop methods of complex neuroprotective therapy, it is necessary to substantiate the targets and tactics of affecting the dendritic tree of the RGCs, the remodeling of which, according to modern concepts, can be closely and antagonistically related to the regeneration of the axon after its damage in trauma and neurodegenerative diseases. RGCs are highly capable of functional modification. Currently, it has been proven that the use of neuroprotective drugs and neurotrophins is promising for maintaining the adaptive plasticity of RGCs and restoring their synaptic contacts at the level of the retina and brain. Understanding the features of the adaptive plasticity of RGCs in AD and glaucoma will make possible to use technologies to activate the internal potential of neuronal remodeling, including the modification of dendritic branching of RGCs and regeneration of their axons, in the preclinical stages of these diseases. Increasing knowledge about the sequence and mechanisms of early events in the retina’s inner plexiform layer will contribute to the development of targeted neuroprotective therapy and new technologies to detect early POAG, AD, and, possibly, other systemic and local neurodegenerative conditions.
Highlights
2021;18(2):198–207 началом, и распространенный вариант — с поздним началом и меньшей привязкой к генетике
which is preceded by a slow period of progressive loss
Recent studies have shown that the integrity of the retinal ganglion cell (RGC)'s dendritic branching can serve as
Summary
Необратимое повреждение структуры аксонов и гибель сомы ганглиозных клеток сетчатки (ГКС) при первичной открытоугольной глаукоме (ПОУГ) и болезни Альцгеймера (БА) развиваются на фоне уже имеющейся клинической манифестации, которой предшествует медленный период прогрессивной потери синапсов и дендритов ГКС. Что целостность дендритного ветвления ГКС может служить и мишенью нейропротекторной терапии, и чувствительным маркером дегенерации сетчатки при БА и глаукоме. Понимание особенностей адаптивной пластичности ГКС при БА и глаукоме позволит использовать в доклинических стадиях этих заболеваний технологии, направленные на активацию внутреннего потенциала ремоделирования нейронов, включая модификацию дендритного ветвления ГК и регенерацию их аксонов. Дендритное ветвление ганглиозных клеток сетчатки как биомаркер глаукомной оптической нейропатии и болезни Альцгеймера и мишень нейропротекторной терапии. Дендритное ветвление ганглиозных клеток сетчатки как биомаркер глаукомной оптической нейропатии. Dendritic Branching of Retinal Ganglion Cells as a Biomarker of Glaucomatous Optic Neuropathy and Alzheimer’s Disease and a Target of Neuroprotective Therapy
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