EA-Tool used binariziation by using the Otsu thresholding algorithm  and Frangi vesselness filter . (SVP), 0.240.12 (ICP), and 0.490.24 (DCP); mean FAZ-R 1.580.94. No correlation was seen for FAZ-R with MD, RNFL, BMO-MRW, RGCL thickness and INL thickness (p 0.05). (II) Substituted piperidines-1 ?2-agAAb have been observed in 91% patients and showed no correlation with MD, RNFL, BMO-MRW, RGCL thickness and INL thickness (p 0.05). (III) Substituted piperidines-1 FAZ-R correlated significantly with the 2-agAAb-induced increase of the beat rate of cardiomyocyte (p = 0.028). Conclusion FAZ characteristics did not correlate with any glaucoma associated functional and morphometric follow-up parameter in the present cohort. However, level of 2-agAAb showed a significantly correlation with FAZ-ratio. We conclude that 2-agAAb might be a novel biomarker in glaucoma pathogenesis showing association to FAZ-ratio with OCT-A. Introduction Glaucoma is known as a multifactorial neurodegenerative disease. The exact pathomechanism is still elusive. Thus, several factors seem to act and interact within this neurodegenerative disorder. Next to an increased intraocular pressure (IOP), being the main risk factor, e.g. oxidative stress , trace elements , an altered trabecular meshwork , immunological  and neuroinflammatory processes  are involved. In addition vascular dysregulation was seen as pathogenetic agent . It is supposed that due to an insufficient nutritive support of retinal ganglion cells via altered microcirculation neurodegeneration could be promoted. A restricted autoregulation with additional vasospasms may enhance this pathophysiologic changes . OCT-angiography (OCT-A) offers the diagnostic option to visualize and quantify retinal microcirculation with subsequent software tools (e.g. Erlangen Angio Tool ). Heidelberg Spectralis II OCT-A (Heidelberg, Germany) is able to scan macular microcirculation in three layers: superficial vascular plexus (SVP, thickness: 80 m), intermediate capillary plexus (ICP, thickness: 50m), and deep capillary plexus (DCP, thickness: 40 m). Substituted piperidines-1 These layers correspond well with anatomical structures : SVP corresponds mainly to the ganglion cell layer (GCL), ICP to the inner plexiform layer (IPL) and inner nuclear layer (INL), and DCP mainly to the outer plexiform layer (OPL, Fig 1). Open in a separate window Fig 1 Structure OCT detail of the macula with the corresponding structural OCT layers and OCT-A slabs of the inner retina (yellow box).Image courtesy by Heidelberg Engineering, Heidelberg, Germany. Substituted piperidines-1 Glaucoma damage focuses on GCL loss, thus, we hypothesize that changes in retinal microcirculation might be accented in SVP and adjacent ICP, potentially most obvious in foveal avascular zone characteristics (FAZ) . A potential link between microvascular retinal alterations and immunological findings in glaucoma might be mirrored by specific agonistic autoantibodies against the ?2-adrenoceptors (?2-agAAb), as ?2-adrenoreceptors (?2-AR) are present on pericytes of retinal microvessels . We observed these ?2-agAAb in a high percentage in sera of patients with primary (POAG), secondary open-angle glaucoma (SOAG) or ocular hypertension (OHT), yet not in controls [12, 13]. The target of ?2-agAAb is additionally present on cells of the trabecular meshwork (TM) and ciliary body [14, 15], both involved in regulation of IOP. Thus, it is assumed that ?2-agAAb might be involved in the pathological increase of IOP via rise of outflow resistance in the TM and increase of production of aqueous humor in the ciliary body. The hypothesis of an increase of outflow resistance is supported by data of Putney et al., describing an increased volume of trabecular meshwork Substituted piperidines-1 cells in patients with glaucoma. The altered cell volume was reportedly TNR induced by osmotic changes due to Na+-K+-Clcotransporters, activated by ?-adrenergic stimulation . Clinical data of a proof-of-principle study supported the hypothesis.