Researchers here report on progress towards non-invasive retinal scanning as an approach to determining Alzheimer's disease risk in the very early stages of progression towards the condition. The path to Alzheimer's is marked by years of a slow accumulation of amyloid-β, an antimicrobial peptide that can misfold to form solid aggregates. While the evidence suggests that amyloid-β can on its own cause mild cognitive impairment, it remains to be determined as to whether it also causes the later stages of Alzheimer's, the chronic inflammation and tau aggregation that kills large numbers of brain cells. It may be a side-effect of other processes, such as persistent viral infection, senescent cell accumulation, and the like. Fortunately, that present lack of knowledge may not matter when it comes to the use of amyloid-β as a marker of risk and progression towards Alzheimer's disease.
Researchers have identified certain regions in the retina - the lining found in the back of the eye - that are more affected by Alzheimer's disease than other areas. The findings were from a clinical trial involving people older than 40 who were showing signs of cognitive decline. In the trial, investigators used a noninvasive technique known as sectoral retinal amyloid imaging to capture retinal images in participants. The retina, which is directly connected to the brain, is the only central nervous system tissue accessible for patient-friendly, high-resolution and noninvasive imaging.
The images were then analyzed using a new process that could identify certain peripheral regions in the retina that corresponded better to brain damage and cognitive status. In studying the images, scientists could detect patients with an increased buildup of retinal amyloid protein, signifying a higher likelihood of developing Alzheimer's disease or cognitive impairments. These findings build upon pioneering research in 2010 in which researchers identified a pathological hallmark of Alzheimer's disease, amyloid beta-protein deposits, in retinal tissues from deceased patients. The team then developed a methodology to detect retinal amyloid beta-protein plaques in living patients suffering from the disease.