Alzheimer's disease (AD) develops undiagnosed for years. Diagnosis of AD remains relatively invasive and restricted to specialized centers calling for development of the new diagnostic markers. Retina may be an attractive source of such markers because it is an accessible part of the CNS (in vivo imaging and electrophysiology). Recent studies indicate pathological alterations in retina of AD patients such as retinal ganglion cell degeneration. Recently, we showed a dysfunction in the glutaminergic photoreceptor synapsis associated with a strong expression of phosphorylated tau proteins (p-tau) in all retina layers in P301S a tauopathic mice model. We demonstrated during our studies that the brain and retinal pathologies are well correlated.During this study we aimed to assess if these features can be generalized to various AD models, especially in a non-human primate model such grey mouse lemur (GML). The GML represents an emerging and promising model in aging neuroscience. They can be AD induced or spontaneously exhibit markers of brain aging and neurodegeneration. It includes age-related cognitive decline, brain atrophy, spontaneous presence of amyloid beta and Tau proteins in about 15% of aged animals.Alterations of visual signal were measured in single retinal ganglion cell obtained ex vivo by multielectrode array recording. The structure of the retina were examined in great detail with respect to the expression of amyloids and p-tau.Our preliminary results showed changes in retinas of some GML during aging with expression of p-tau, amyloids and changes in the synaptic responses. The induced AD-GML showed high expression of Ab and p-Tau.