Abstract
In Alzheimer’s disease (AD), vascular changes could be caused by amyloid beta (Aβ) aggregates replacing the contractile smooth musculature of the arteriole walls. These changes happen in the brain vascular network, but also in the eye, and are related to decreased vascular density and low blood flow. In patients with Alzheimer’s disease, thinning of the choroid and the retina has been shown. The aim of this prospective study was to assess the retinal and choroidal vascular systems, analyzing the choroidal thickness with optical coherence tomography (OCT), the foveal avascular zone (FAZ) with OCT-angiography (OCTA), and the optic nerve head (ONH) hemoglobin with the Laguna ONhE program, to evaluate which of the two ocular vascular systems shows earlier changes in mild AD patients. These patients, compared to controls, showed a significantly thinner choroid at all the analyzed points, with the exception of the temporal macula (at 1000 and 1500 µm from the fovea). On the other hand, the FAZ and ONH hemoglobin did not show significant differences. In conclusion, a thinner choroid was the main ocular vascular change observed in mild AD patients, while the retinal vessels were not yet affected. Therefore, choroidal thickness could be used an early biomarker in AD.
Highlights
Cerebral amyloid angiopathy, present in 90% of patients with Alzheimer’s disease (AD), is one of the earliest pathological signs of the development of the disease [1,2]
The inner retina is supplied by blood vessels derived from the central retinal artery (CRA) [16], and its capillaries have a high 1:1 endothelial/pericyte ratio [17] that helps to regulate the blood supply
In order to facilitate the passage of nutrients into the retina, the pericytes do not surround the capillary in this choroidal layer, appearing only towards the scleral side at an endothelial cells/pericytes ratio of 6:1 [18]
Summary
Present in 90% of patients with Alzheimer’s disease (AD), is one of the earliest pathological signs of the development of the disease [1,2]. The loss of smooth muscle cells disrupts the normal functioning of the neurovascular unit, with the regulation of local blood flow worsening due to a loss of vascular contractibility and a partial occlusion in the smaller distal arterioles by Aβ aggregates [8]. These changes have been associated with decreases in vascular density, vascular thickness, and blood flow in the brain [9]. Given the contractile capacity of the pericytes, the low proportion of pericytes in the choriocapillaris might suggest that in the regulation of the choroidal blood flow, other regulatory mechanisms would intervene, such as the autonomic nervous system [18,19]
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