Bace1−/− mice display retinal pathology (Cai et al, 2012) and changes in NRG1 signaling, leading to a schizophrenia-like phenotype (Savonenko et al, 2008) and impaired formation of muscle spindles (Cheret et al, 2013).
To investigate the role of CX3CR1 in microglial function during DR, we crossed Insulin2 Akita (Ins2 Akita) mice, with CX3CR1-knockout (KO) mice, to study retinal pathology in nondiabetic and diabetic (Ins2 Akita), wild type (WT or heterozygous [HET]), and CX3CR1-KO mice.
Here we show that BACE1−/− mice develop significant retinal pathology including retinal thinning, apoptosis, reduced retinal vascular density and an increase in the age pigment, lipofuscin.
RESULTS: β-Secretase knockout mice develop significant retinal pathology including retinal thinning, vascular abnormalities and an increase in the age pigment, lipofuscin.
Since these mice were reported to show retinal pathology at advanced age [ 20, 22], we investigated 16-month-old Cln3 -/- mice and Cln3 +/+ control littermates.
Altogether, these data can be instrumental to study MMP expression in mouse models of retinal pathologies.
The purposes of this study were to determine whether NRF2-deficient mice would develop AMD-like retinal pathology with aging and to explore the underlying mechanisms.
In summary, our study demonstrated that mice deficient in NRF2 presented retinal pathology of age-related drusen formation, RPE/BrM degeneration, sub-RPE deposition of inflammatory proteins and spontaneous CNV, all of which are key features of human AMD.
The present study clarifies primary and secondary confounding effects of the Crb1 rd8/rd8 mutation on retinal pathology in mice.
To establish the contribution of the genetic background to phenotypic variability associated with the Crb1 rd8/rd8 mutation, we compared the retinal pathology of Crb1 rd8/rd8/J inbred mice with that of two Crb1 rd8/rd8 lines backcrossed with C57BL/6JOlaHsd mice.
