TY - JOUR T1 - Longitudinal Brain FDG PET Profiles Displaying Neuron Secondary Degeneration in the Visual Pathway in An Optic Nerve Crush(ONC) Rat Model <strong/> JF - Journal of Nuclear Medicine JO - J Nucl Med SP - 80 LP - 80 VL - 61 IS - supplement 1 AU - Weiyan Zhou AU - Xiang Shi AU - Qi Huang AU - Yihui Guan Y1 - 2020/05/01 UR - http://jnm.snmjournals.org/content/61/supplement_1/80.abstract N2 - 80Purpose: Glaucoma is an irreversible blinding disease characterized by progressive atrophy of the optic nerve and varying degrees of visual field loss. Researchers assumed glaucoma could be considered as a progressive neurodegenerative condition spreading throughout the brain. Mouse models of optic nerve crush(ONC) are used as a typical in vivo model of glaucoma. In the visual pathway, ONC may cause secondary degeneration of neurons in distal regions, such as the visual cortex. However, the mechanisms of neuron impairment in the visual cortex after ONC remains unclear. In the present study, we aimed to investigate the longitudinal brain metabolic changes in adolescent rats following bilateral optic nerve crush using small animal positron emission tomography (PET). Methods: 2-Deoxy-2-[18F]Fluoro-D-glucose([18F]FDG) microPET imaging was performed at the 1th, 3th and 10th days after modeling, and statistical parametric mapping (SPM) was used for image analysis. NeuN and TUNEL staining were performed for neuron loss and apoptosis. And GFAP and Iba1 were stained to evaluate the neuroinflammatory response. Results: Cerebral glucose metabolism was decreased in the bilateral visual cortex and the left lateral geniculate nucleus at the first day after modeling but without obvious inflammatory cell activation or nerve cell necrosis. On the 3rd day, FDG metabolism declined in the bilateral visual cortex and thalamus extensively, on the contrary, the extent and range of decreased FDG uptake in the above-mentioned brain regions was alleviated on the 10th day. Astrocytes and microglias were significantly activated in the primary visual cortex (V1) and the visual thalamus as a response to ONC, while they peaked on the 10rd day. Visual electrophysiological function was worsened 1 days-10 days after ONC. Conclusions: [18F]FDG microPET brain imaging study in combination with immunohistological investigation revealed that neuron apoptosis and neuroinflammation were might specifically involved in the neuromechanism of adolescent glaucoma. Brain FDG PET could provided valuable insights into the second neuro-degeneration even before the neuropathology occurred in the CNS. Alleviation of the impaired FDG uptake in the involved brain cortex and subcortical gray matter during the late stage might be explained by neuroplasticity. Taken together, these findings suggest that that traditional intraocular pressure(IOP)-lowering therapies are often not sufficient to prevent progression to blindness and neuroprotection strategies should be under consideration and initiated at the disease onset. ER -