Umur Kayabasi1 and John Rose Sr. 2
Recent research suggests that Tau is the offender injury alongside neuroinflammation in the etiology of Alzheimer’s disease (AD). Retina is the extention of the brain and is the most easily approachable part of the central nervous system. Disclosure of the neurotic protein aggregations might be conceivable by utilizing otherworldly space optical coherescent tomography ( SD-OCT ) and fundus autofluorescein ( FAF ). There is evidence showing that retinal plaques start accumulating even earlier than the ones in the brain. Most new Tau protein images in the brain consist of normal or reverse C-shaped paired hellical filaments. Tau is an axon-enhanced protein that ties to and settles microtubules, and subsequently assumes a critical job in neuronal capacity. In Alzheimer's ailment (AD), neurotic tau collection relates with psychological decrease. Generous visual shortfalls are found in people influenced by AD including a special loss of retinal ganglion cells (RGCs), the neurons that pass on visual data from the retina to the mind. At present, be that as it may, the components that underlie vision changes in these patients are inadequately comprehended. Here, we asked whether tau assumes a job in early retinal pathology and neuronal brokenness in AD.