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The Retinal Inner Plexiform Synaptic Layer Mirrors Grey Matter Thickness of Primary Visual Cortex with Increased Amyloid β Load in Early Alzheimer’s Disease
Neural Plasticity ( IF 3.1 ) Pub Date : 2020-09-21 , DOI: 10.1155/2020/8826087
Lília Jorge 1, 2 , Nádia Canário 1, 2 , Ricardo Martins 1, 2 , Beatriz Santiago 3, 4, 5 , Isabel Santana 3, 4, 5 , Hugo Quental 1, 2, 4 , Francisco Ambrósio 3, 4, 5, 6 , Rui Bernardes 1, 2, 3 , Miguel Castelo-Branco 1, 2, 3
Affiliation  

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.

中文翻译:

视网膜内丛状突触层反映了早期阿尔茨海默病中淀粉样蛋白 β 负载增加的初级视觉皮层的灰质厚度

视网膜可以作为阿尔茨海默病 (AD) 突触丧失神经病理学的推定窗口。在这里,我们研究了富含突触的层与 AD 早期由细胞核/细胞体组成的层。此外,我们检查了视网膜变化与皮质损伤的分子和结构标志物之间的关联。我们招募了 20 名 AD 患者和 17 名健康对照 (HC)。组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,我们测量的视网膜和视觉皮层(V1)的厚度,随着V1的淀粉样蛋白β(A β) 保留([11C]-PiB PET 示踪剂)和神经炎症([11C]-PK11195 PET 示踪剂)。我们发现,在没有神经炎症的情况下,V1 显示出增加的淀粉样蛋白结合潜力。尽管仍然没有厚度变化,但我们发现 AD 中富含突触的内丛状层 (IPL) 和 V1 之间存在正相关。此retinocortical相互作用可能反映在从A所得突触功能的变化β的沉积,从而有助于早期的视觉损失。
更新日期:2020-09-21
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