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Editors Selection IGR 18-1
Basic Science: Effects of IOP on Cognitive Function in Rats
Comment by Luciano Quaranta on:
74344 High intraocular pressure produces learning and memory impairments in rats, Yuan Y; Chen Z; Li L et al., Brain Research, 2017; 1675: 78-86
The results of the present study show that high IOP impaired learning and memory in ocular hypertension model in rats and concurrently increased β-amyloid (Aβ) and phospho-tau expression in the hippocampus by altering the activation of different kinase and phosphatase proteins in the hippocampus. This study provides novel suggestion for the relationship between high IOP and hippocampal alterations, especially in the context of learning and memory.
There is evidence suggesting that glaucoma also affects other components of the visual pathway. Glaucomatous neuronal death occurs in the retina, optic nerve, lateral geniculate nucleus (LGN), and the visual cortex. Neuropathologic examination revealed marked degenerative changes, including neuron shrinkage and loss in the LGN, which was accompanied by reactive astrogliosis or glial activation.4 Magnetic resonance (MR) techniques are well suited for evaluating the brain changes in vivo. Moreover, studies have demonstrated decreases in LGN volume25and visual cortex thickness. Functional MR showed decreased response in the visual cortex after stimulation of the glaucomatous eye. Therefore, these mechanisms are similar to those first described in neuro-degenerative diseases, which comprise a heterogeneous group of disorders with clinical and pathologic diversity, including Alzheimer's disease (AD), Parkinson's disease, and amyotrophic lateral sclerosis.
The clinical and pathologic relationship between AD and glaucoma remains obscureOther investigations on chronic glaucoma model in rhesus monkeys, have shown that distribution of AD-like pathology along the visual pathway occurred in an ascending order without being observed in cognitive areas, particularly the Hyppocampus, indicates that IOP elevation may produce damage to the glaucomatous central visual system via axonal and synaptic changes.
No consensus has been established regarding whether clinical correlations between the two diseases might be due to shared risk factors or the influence of one disorder on the other, and different mechanisms may trigger the biomolecular processes leading to cell death in these diseases. These observations raise the intriguing possibility that underlying AD-like pathology contributes to the visual impairment due to glaucoma. Studying these pathologies may result in a paradigm shift in the management of ocular diseases. It has been shown that targeting different components of the β-amyloid formation and aggregation pathway can reduce glaucomatous retinal ganglion cells apoptosis in vivo and, therefore, raises the possibility of using neuroprotective mechanisms to combat glaucoma.
The clinical and pathologic relationship between AD and glaucoma remains obscure.
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