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Brain aging is associated with cognitive decline that is accompanied by progressive neuroinflammatory changes. The endocannabinoid system (ECS) is involved in the regulation of glial activity and influences the progression of age-related learning and memory deficits. Mice lacking the Cnr1 gene (Cnr1 −/− ), which encodes the cannabinoid receptor 1 (CB1), showed an accelerated agedependent deficit in spatial learning accompanied by a loss of principal neurons in the hippocampus. The age-dependent decrease in neuronal numbers in Cnr1 −/− mice was not related to decreased neurogenesis or to epileptic seizures. However, enhanced neuroinflammation characterized by an increased density of astrocytes and activated microglia as well as an enhanced expression of the inflammatory cytokine IL-6 during aging was present in the hippocampus of Cnr1 −/− mice. The ongoing process of pyramidal cell degeneration and neuroinflammation can exacerbate each other and both contribute to the cognitive deficits. Deletion of CB1 receptors from the forebrain GABAergic, but not from the glutamatergic neurons, led to a similar neuronal loss and increased neuroinflammation in the hippocampus as observed in animals lacking CB1 receptors in all cells. Our results suggest that CB1 receptor activity on hippocampal GABAergic neurons protects against age-dependent cognitive decline by reducing pyramidal cell degeneration and neuroinflammation.glial regulation | Morris water maze | stereological quantification | CD40 expression | telemetric EEG recording

The present study investigated the changes in several erythrocyte oxidative stress biomarkers in hypoxic elderly individuals to analyze the deleterious effects of low oxyhemoglobin saturation in an elderly population. We collected blood samples from one normoxic middle-aged group and two groups composed of individuals older than 75 years of age: one normoxic group and one hypoxic group. Aging appeared to provoke a defective erythrocyte antioxidant defense associated with increased oxidative damage in the elderly population. Acute hypoxia activated an insufficient antioxidant defense response as suggested by the oxidative damage observed. The oxidative imbalance presented in older participants and increased in hypoxia participants had a direct effect on glyceraldehyde-3-phosphate dehydrogenase cell distribution. Oxidative stress levels altered Band 3 protein and mediated caspase-3 activation in erythrocyte from the aged group although it was not extended to hypoxic individuals. Therefore, aged participants appeared to activate an insufficient antioxidant response against hypoxia-related oxidative stress.

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