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. 2020 Sep 21:2020:8826087.
doi: 10.1155/2020/8826087. eCollection 2020.

The Retinal Inner Plexiform Synaptic Layer Mirrors Grey Matter Thickness of Primary Visual Cortex with Increased Amyloid β Load in Early Alzheimer's Disease

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
Affiliations

The Retinal Inner Plexiform Synaptic Layer Mirrors Grey Matter Thickness of Primary Visual Cortex with Increased Amyloid β Load in Early Alzheimer's Disease

Lília Jorge et al. Neural Plast. .

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.

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Conflict of interest statement

The authors have no conflict of interest to report.

Figures

Figure 1
Figure 1
Resulting cortical thickness map between HC and AD groups, with the representation of the V1 area: (a) right hemisphere, (b) left hemisphere.
Figure 2
Figure 2
Macular image resulting from the segmentation, identifying the layers analyzed in this study. GCL: ganglion cell layer; IPL: inner plexiform layer; INL: inner nuclear layer; OPL: outer plexiform layer.
Figure 3
Figure 3
V1 measurements in 20 AD patients compared to 17 HC. (a) [11C]-PiB SUVR; (b) [11C]-PK1195 BPND; (c) V1 thickness. There is a significant difference in the mean of [11C]-PiB SUVR (a) between groups, but not in [11C]-PK1195 BPND (b) or in V1 thickness (c).
Figure 4
Figure 4
Scatterplot graph for the V1 thickness and IPL thickness to HC and AD.
See this image and copyright information in PMC

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References

    1. Avila J., Pallas N., Bolós M., Sayas C. L., Hernandez F. Intracellular and extracellular microtubule associated protein tau as a therapeutic target in Alzheimer disease and other tauopathies. Expert Opinion on Therapeutic Targets. 2015;20(6):653–661. doi: 10.1517/14728222.2016.1131269. - DOI - PubMed
    1. Bloom G. S. Amyloid-β and tau the trigger and bullet in Alzheimer disease pathogenesis. JAMA Neurology. 2014;71(4):505–508. doi: 10.1001/jamaneurol.2013.5847. - DOI - PubMed
    1. Hardy J., Selkoe D. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science. 2002;297(5580):353–356. doi: 10.1126/science.1072994. - DOI - PubMed
    1. Oliveira L. T., Louzada P. R., de Mello F. G., Ferreira S. T. Amyloid-β decreases nitric oxide production in cultured retinal neurons: a possible mechanism for synaptic dysfunction in Alzheimer’s disease? Neurochemical Research. 2011;36(1):163–169. doi: 10.1007/s11064-010-0287-z. - DOI - PubMed
    1. Pasqualetti G., Brooks D. J., Edison P. The role of neuroinflammation in dementias. Current Neurology and Neuroscience Reports. 2015;15(4):p. 17. doi: 10.1007/s11910-015-0531-7. - DOI - PubMed

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