Retinal microvascular attenuation in mental cognitive impairment and Alzheimer's disease by optical coherence tomography angiography

Purpose To explore regional variation of the macular microvasculature in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD), also to detect the association between retinal macular microvascular parameters and the progress of preclinical AD. Methods Prospective study of healthy controls, patients with MCI and patients with AD by using Optical coherence tomography angiography (OCT-A). We quantified foveal avascular zone (FAZ) areas, densities of the superficial retinal capillary plexuses (SRCP) and deep retinal capillary plexuses (DRCP). The SRCP and DRCP were divided into inner (3 mm) and external (6 mm) annular rings, each containing four quadrants (SI, II, TI, NI, SE, IE, TE and NE). The data were analysed statistically by using SPSS 22 software. Results Totally, 60 subjects including 21 HC (33 eyes), 21 patients with MCI (32 eyes) and 18 AD patients (28 eyes) were recruited. The microvascular densities of DRCP at all quadrants of the parafovea and perifovea were significantly lower in AD patients compared to HC group (p < 0.05). Compared to the HCs, MCI patients showed significant microvascular loss in most sectors of the parafovea and the SE sector of the DRCP (p < 0.05), but not in the parafovea (p = 0.829) or perifovea (p = 0.824) of the SRCP. No significant difference was found in microvascular density of SRCP among the groups, except at SI between the AD and HC groups (p = 0.048). Conclusion Our findings demonstrated the macular microvascular attenuation in MCI and AD patients. Both AD and MCI patients showed retinal microvascular density loss, which is more significant in the deep retinal capillary plexuses. Optical coherence tomography angiography (OCT-A) can be used to identify early microvascular abnormalities in AD and MCI. Quantified microvascular density in the DRCP might serve as potential biomarkers of early sign of AD then contribute to forestall the progression of preclinical AD.