Abstract
Purpose:
While Alzheimer’s disease (AD) patients are known to experience histological retinal changes, the thalamic intermediaries connecting eye and cortex have been understudied. We wanted to examine whether Alzheimer's disease (AD) biomarkers are expressed in the normal human lateral geniculate nucleus (LGN) and whether AD alters the presence of these markers. We also wanted to determine whether these markers are expressed in pre-clinical AD.
Methods:
Following IRB approval, we obtained human tissue samples from the Maryland Brain and Tissue Bank. These included normal, pre-clinical, and severe AD. We immunohistochemically evaluated human LGN for the expression of both AD markers (phosphorylated tau, amyloid precursor protein (APP) and amyloid-β (Aβ)) and inflammation using standard immunohistochemistry (IHC) procedures. Cellular inflammation was compared using IBA1. Slides were analyzed using a confocal fluorescent microscope and Fluoview Software.
Results:
While normal tissue showed minimal expression of AD biomarkers, there was a progressive increase in Tau, Aβ, APP, and inflammation in the lateral geniculate nucleus through the different stages of AD severity. Interestingly, the inflammatory response and deposits of AD biomarkers were shown in significant amounts in the pre-clinical AD samples of the LGN.
Conclusions:
The LGN-thalamic structure shows AD-induced alterations as the disease progresses and very early in the disease process. This may result in a decreased ability to process visual information, and visual problems. The presence of inflammation and AD-related biomarkers in pre-clinical AD patients suggests that for at least some older adults, changes in visual processing ability and speed may be due to AD onset, and not normal age-related visual decline.
Keywords: 413 aging •
638 pathology: human •
554 immunohistochemistry