Citation

Saccà SC, Cutolo CA, Rossi T. Subcell. Biochem. 2019; 91: 393-434.

Affiliation

Department of Head/Neck Pathologies, St Martino Hospital, Ophthalmology Unit, Genoa, Italy.

Copyright

(Copyright © 2019, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/978-981-13-3681-2_14

PMID

30888660

Abstract

Many diseases are related to age, among these neurodegeneration is particularly important. Alzheimer's disease Parkinson's and Glaucoma have many common pathogenic events including oxidative damage, Mitochondrial dysfunction, endothelial alterations and changes in the visual field. These are well known in the case of glaucoma, less in the case of neurodegeneration of the brain. Many other molecular aspects are common, such as the role of endoplasmic reticulum autophagy and neuronal apoptosis while others have been neglected due to lack of space such as inflammatory cytokine or miRNA. Moreover, the loss of specific neuronal populations, the induction of similar mechanisms of cell injury and the deposition of protein aggregates in specific anatomical areas are very similar events between these diseases. Intracellular and/or extracellular accumulation of protein aggregates is a key feature of many neurodegenerative disorders. The existence of abnormal protein aggregates has been documented in the RGCs of glaucomatous patients such as the anomalous Tau protein or the β-amyloid accumulations. Intra-cell catabolic processes also appear to be common in both glaucoma and neurodegeneration. They also help us to understand how the basis between these diseases is common and how the visual aspects can be a serious problem for those who are affected.

Language: en

Keywords

Alzheimer’s disease; Autophagy; Endothelial dysfunction; Glaucoma; Mitochondria; Oxidative stress; Parkinson’s disease; Trabecular meshwork; Visual field