Abstract
The retina may serve as putative window into neuropathology of synaptic loss in Alzheimer's disease (AD). Here, we investigated synapse-rich layers versus layers composed by nuclei/cell bodies in an early stage of AD. In addition, we examined the associations between retinal changes and molecular and structural markers of cortical damage. We recruited 20 AD patients and 17 healthy controls (HC). Combining optical coherence tomography (OCT), magnetic resonance (MR), and positron emission tomography (PET) imaging, we measured retinal and primary visual cortex (V1) thicknesses, along with V1 amyloid β (Aβ) retention ([11C]-PiB PET tracer) and neuroinflammation ([11C]-PK11195 PET tracer). We found that V1 showed increased amyloid-binding potential, in the absence of neuroinflammation. Although thickness changes were still absent, we identified a positive association between the synapse-rich inner plexiform layer (IPL) and V1 in AD. This retinocortical interplay might reflect changes in synaptic function resulting from Aβ deposition, contributing to early visual loss.
Highlights
Alzheimer’s disease is characterized by the presence of abnormal extracellular amyloid β (Aβ) toxic deposits causing synaptic dysfunction, putative neuroinflammation due to microglia activation, and neuronal loss [1,2,3,4,5,6], which typically lead to progressive brain atrophy.The impact of this pathology in the retina as well as other parts of the visual system in AD remains to be understood [7]
We studied the structural integrity of 4 layers, 2 composed by synapses—inner plexiform layer (IPL) and outer plexiform layer (OPL)—and 2 composed by cell bodies—ganglion cell layer (GCL) and inner nuclear layer (INL), the layers of the inner retina closer to the brain
We were able to test whether in an early stage of the AD, the neuropathological mechanisms of the disease differently affects the integrity of retinal layers with distinct dominance of either synapses or cell bodies/nuclei between patients and healthy controls, matched for age, education, and sex
Summary
Alzheimer’s disease is characterized by the presence of abnormal extracellular Aβ toxic deposits causing synaptic dysfunction, putative neuroinflammation due to microglia activation, and neuronal loss [1,2,3,4,5,6], which typically lead to progressive brain atrophy The impact of this pathology in the retina as well as other parts of the visual system in AD remains to be understood [7]. As a part of the central nervous system (CNS), the retina shares multiple features with the brain, in terms of embryological development, anatomy, and function [32,33,34,35] These similarities along with the visual changes observed in patients
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