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Objective. Retinal injury induced by ethanol consumption has been previously reported in animal models, including biochemical, histological and functional alterations. These results need to be clinically tested in alcoholic patients which do not report several systemic or ophthalmic diseases. Methods. Six patients with alcohol use disorder were recruited from an ‘Alcoholism Treatment Unit’. All of them with active alcohol consumption when the study was conducted or that had stopped drinking six months prior to the study, with no ocular disease or visual acuity alterations. All patients underwent fundus photography, optical coherence tomography (OCT) as well as visual field test. Electrophysiological tests were conducted to check retinal function: Ganzfeld Electroretinogram (ERG), Pattern Electroretinogram (PERG), Multifocal Electroretinogram (mfERG), and also Visual Evoked Potential (VEP). Results.Visual acuity was normal in all cases as well as fundus photography and visual field test. The OCT showed a mild decrease in the retinal nerve fiber layer thickness average in three patients. Five patients showed impairments in mfERG response, decreased amplitude in ERG response and no significant alterations in PERG and VEP. Conclusion. Although standard ophthalmic tests did not show signs of an ocular disease, the study of electrical function showed different impairments in almost all patients. The alterations reported in mfERG and ERG recordings could reflect inner retina injury, thus supporting the possible existence of an alcoholic retinopathy. Further studies with larger number of subjects are necessary to assess the specific impact of other factors such as tobacco or nutritional status on patients with alcohol use disorder. Sin financiación No data JCR 2019 0.497 SJR (2019) Q2, 262/545 Psychiatry and Mental Health, 126/295 Clinical Psychology No data IDR 2019 UEV

Diabetes mellitus is a common metabolic disorder associated with chronic complications including a state of mild to moderate cognitive impairment, in particular psychomotor slowing and reduced mental flexibility, not attributable to other causes, and shares many symptoms that are best described as accelerated brain ageing. A common theory for aging and for the pathogenesis of this cerebral dysfunctioning in diabetes relates cell death to oxidative stress in strong association to inflammation, and in fact nuclear factor κB (NFκB), a master regulator of inflammation and also a sensor of oxidative stress, has a strategic position at the crossroad between oxidative stress and inflammation. Moreover, metabolic inflammation is, in turn, related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect. In parallel, blockade of autophagy can relate to proinflammatory signaling via oxidative stress pathway and NFκB-mediated inflammation.