|
| Ocular hallmarks in experimental animal models |
| Ref. | Model | Findings |
|
| Oliveira-Souza et al. 2017 [108] | Tg-SwDI mice
6.5 to 15 months | Upregulation of AChR gene expression and significant cell loss in the photoreceptor layer and inner retina on young groups. Specific cholinergic cell loss and increased astrocytic gliosis in the middle-aged and AChR downregulation in older adult groups. |
| Joly et al. 2017 [209] | Tg APPswe/PS1DE9 mice
3 to 13 months | No Aβ or amyloid plaques were detected in the Tg retinas. However, the CTFb/CTFa ratio was significantly lower. Response mediated by cones was preserved. Retinal-specific processing of amyloid may confer protection against AD and selectively preserve cone-dependent vision during aging. |
| Nilson et al. 2017 [73] | P301L mouse
Htau mouse | Tau oligomers colocalize with astrocytes, microglia, HMGB1, and inflammatory cells in the retina. |
| Chiasseu et al. 2017 [74] | 3xTg mice
3 to 6 months | Age-related increase in endogenous retinal tau accumulation, previous to the reported onset of behavioral deficits, and tau aggregation in the brain. Tau build-up occurred in GCL soma and dendrites, but not in axons. |
| Chidlow et al. 2017 [56] | Tg APPSWE/PS1ΔE9 mouse
3 to 12 months | No presence of amyloid plaques, dystrophic neurites, neuronal loss, macro- or microgliosis, OS, tau hyperphosphorylation, or upregulations of proinflammatory cytokines in the retina. |
| Gupta et al. 2016 [47] | Tg APP/PS1 mice
13 to 16 months | Increased Aβ deposition in the retinas with thinning in inner retinal layers and decline in scotopic threshold response. Reduction of axonal density in the optic nerve. |
| Du et al. 2015 [65] | Octodon degus
6.7–70 months | Aβ deposition in the inner and outer segment of the photoreceptors, NFL, and GCL. Aβ expression was higher in the central retinal region than in the retinal periphery. Phosphorylated tau was seen more consistently in NFL-GCL regardless of age. |
| Pogue et al. 2015 [80] | Tg 5xFAD Tg-AD mice
0–5 months | Presence of Aβ42 peptides in the brain and retina, accompanied by inflammatory markers such as cyclooxygenase-2 and C-protein reactive. |
| Maharshak et al. 2016 [90] | ApoE3 and ApoE4 targeted replacement mice
4–7–12–120 days old | Transient changes in vascular branching and decrease in retinal synaptic density in the apoE4 mice. Additionally, lower levels of retinal VEGF were observed in apoE4 mice compared to the ApoE3 mouse retinas. |
| Tsai et al. 2014 [67] | TgF344-AD rat
14–19 months | Reduction in choroidal thickness, hypertrophic retinal pigment epithelial cells, inflammatory cells, Aβ plaques, and upregulation of complement factor C3 in the retina. |
| Williams et al. 2013 [210] | Tg 2576 mice
14 months | No significant changes in GCL synaptic densities but a highly significant change in mitochondrial morphology. GCL dendritic atrophy preceded cell loss, and this may be due to the accumulations of Aβ. |
| Zhao et al. 2013 [76] | Tg APP/PS1 mice | Hyperexpression of phosphorylated tau was detected in retina, accompanied with an increase in senile plaques and NFTs. The increased tau phosphorylation was associated with a significant augment in the production of p35 and p25, and upregulation of calpain. |
| Schon et al. 2012 [77] | Tg P301S mice | In vivo detection of fibrillar tau in the retina and the progression of tau pathology over several months was demonstrated. |
| Koronyo-Hamaoui et al. 2011 [66] | Tg APPSWE/PS1ΔE9 mouse
7–17 months | Retinal Aβ plaques were detected following systemic administration of curcumin in Tg, previous to the appearance of Aβ plaques in the brain. |
| Perez et al. 2009 [64] | Tg APPSWE/PS1DeltaE9 mouse
12–19 months | Aβ plaques appeared in the OPL and IPL of the retina, displaying syntaxin 1 and ChAT, but no neuronal degeneration was observed. ERG revealed reduction in the amplitudes of a and b waves. |
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