Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra, Coimbra, Portugal.
Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra, Coimbra, Portugal.
Neural Plast. 2020 Sep 21;2020:8826087. doi: 10.1155/2020/8826087. eCollection 2020.
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 (A) 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 A deposition, contributing to early visual loss.
视网膜可能是阿尔茨海默病(AD)突触丢失神经病理学的潜在窗口。在这里,我们研究了 AD 早期富含突触的层与由核/细胞体组成的层。此外,我们还研究了视网膜变化与皮质损伤的分子和结构标志物之间的关系。我们招募了 20 名 AD 患者和 17 名健康对照者(HC)。结合光学相干断层扫描(OCT)、磁共振(MR)和正电子发射断层扫描(PET)成像,我们测量了视网膜和初级视觉皮层(V1)的厚度,以及 V1 淀粉样蛋白(A)保留([11C]-PiB PET 示踪剂)和神经炎症([11C]-PK11195 PET 示踪剂)。我们发现 V1 显示出淀粉样蛋白结合能力增加,而没有神经炎症。尽管厚度变化仍然不存在,但我们在 AD 中发现了富含突触的内丛状层(IPL)与 V1 之间的正相关。这种视网膜-皮质相互作用可能反映了由于 A 沉积导致的突触功能变化,导致早期视觉丧失。