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Invest Ophthalmol Vis Sci. 2017 Oct 1;58(12):5434-5443. doi: 10.1167/iovs.17-22312.

Elevated Intraocular Pressure Induces Amyloid-β Deposition and Tauopathy in the Lateral Geniculate Nucleus in a Monkey Model of Glaucoma.

Author information

1
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, People's Republic of China.
2
Department of Ophthalmology, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, People's Republic of China.
3
Department of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, People's Republic of China.
4
Department of Ophthalmology, The Third People's Hospital of Huizhou, Huizhou, People's Republic of China.

Abstract

Purpose:

Recent evidence has suggested a potential association between Alzheimer's disease (AD) and glaucoma and found significant deposition of amyloid-β (Aβ) and Tau protein in the retinas of glaucoma patients. However, no coherent finding has emerged regarding the AD-like changes in the central visual system (CVS). Studies confirming the presence of Aβ and Tau neuropathology are warranted to identify the underlying mechanism that contributes to the visual impairment observed in glaucoma.

Methods:

A chronic glaucoma model was established in rhesus monkeys. The retina, optic nerve, CVS including the lateral geniculate nucleus (LGN) and primary visual cortex (V1), and cognitive areas including the hippocampus (Hpp) were evaluated. Aβ 1-42 and phosphorylated-Tau (p-Tau) were tested in the aforementioned structure using immunohistochemistry, Western blotting and ELISA, and the neuritic plaques and argyrophilic structures/neurofilaments were observed using silver staining and transmission electron microscopy (TEM).

Results:

Immunohistochemistry revealed positive Aβ and p-Tau labeling in the LGN. According to Western blotting assay and ELISA, Aβ and p-Tau were present in the LGN. Aβ also was expressed weakly in the primary visual cortex. In contrast, the hippocampus, which is the most severely affected region in AD, showed no positive labeling. Structurally, silver staining and TEM revealed neuritic plaques and argyrophilic structures/neurofibrillary tangles, in the LGN.

Conclusions:

For the first time to our knowledge, these data collectively establish the existence of hallmark AD-like pathologies in the glaucomatous LGN. Our results may provide new targets for developing research therapies that will enhance neuroprotection in glaucoma patients.

PMID:
29059309
DOI:
10.1167/iovs.17-22312
[Indexed for MEDLINE]

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