Purpose: To detect early diabetic damage in type 2 diabetes mellitus patients with no diabetic retinopathy (NDR) using optical coherence tomography (OCT) and to evaluate OCT as a clinical test. Methods: Thirty-two patients with NDR (n = 32) were enrolled. We examined retinal and retinal nerve fiber layer (RNFL) thickness using OCT. Two healthy normal populations were also enrolled for the retinal thickness (n = 48) and RNFL thickness (n = 34). Both OCT measurements were obtained in four areas (temporal, superior, nasal and inferior). The receiver operator characteristic (ROC) curve was generated to evaluate the predictor variables. Results: Comparing the normal and NDR eyes, retinal thickness significantly increased (p = 0.03) and RNFL thickness significantly decreased (p = 0.02) in the superior areas. The area under the ROC curve was 0.65 for the superior retinal thickness and 0.63 for the superior RNFL thickness. Conclusions: Both OCT measurements can detect early retinal damage in NDR patients.

Angiogenesis is a prominent feature of central nervous system (CNS) disease and has roles in both the continued promotion of inflammation and the subsequent repair processes. Here we report that prostacyclin (or prostaglandin I(2) (PGI(2))) derived from new vessels promotes axonal remodeling of injured neuronal networks after CNS inflammation. In a localized model of experimental autoimmune encephalomyelitis (EAE), new vessels formed around the inflammatory lesion, followed by sprouting of adjacent corticospinal tract (CST) fibers. These sprouting fibers formed a compensatory motor circuit, leading to recovery of motor function. Capillary endothelial cell-derived prostacyclin bound to its receptor, the type I prostaglandin receptor (IP receptor), on CST neurons, promoting sprouting of CST fibers and contributing to the repair process. Inhibition of prostacyclin receptor signaling impaired motor recovery, whereas the IP receptor agonist iloprost promoted axonal remodeling and motor recovery after the induction of EAE. These findings reveal an important function of angiogenesis in neuronal rewiring and suggest that prostacyclin is a promising molecule for enhancing functional recovery from CNS disease.

Background: Pericyte damage is closely associated with the progression of neurodegeneration and neuronal dysfunction in the central nervous system (CNS). Results: Prostacyclin attenuates pericyte damage following vascular barrier dysfunction in the adult CNS. Conclusion: Prostacyclin therapy diminishes demyelination and neuronal deficits in pathophysiological conditions. Significance: This study provides the first evidence that pericyte protection contributes to attenuate disease progression in adult CNS.