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IBBR publication #2017

Conjugated linoleic acid prevents age-dependent neurodegeneration in a mouse model of neuropsychiatric lupus via the activation of an adaptive response

Monaco A, Ferrandino I, Boscaino F, Cocca E, Cigliano L, Maurano F, Luongo D, Spagnuolo MS, Rossi M, Bergamo P

Journal of Lipid Research 59 (1): 48-57. (2018)
doi: 10.1194/jlr.M079400

Oxidative stress is a key mediator of autoimmune/neurodegenerative disorders. The antioxidant/anti-inflammatory effect of a synthetic conjugated linoleic acid (CLA) mixture in MRL/MpJ-Faslpr mice (MRL/lpr), an animal model of neuropsychiatric lupus, was previously associated with the improvement of Nuclear factor-E2-related factor 2 (Nrf2) defences in the spleen and liver. However, little is known about the neuroprotective ability of CLA mixture. This study investigates the age-dependent progression of oxidative stress and the hyperactivation of redox-sensitive compensatory pathways (macroautophagy, Nrf2) in old/diseased MRL/lpr mice brains, and examines the effect produced by dietary CLA supplementation. Disrupted redox homeostasis was evidenced in the blood, liver and brain of 21- to 22-week old MRL/lpr mice (Old) compared to young animals (Y; 8- to 10-week old). This alteration was associated with significant hyperactivation of compensatory mechanisms (macroautophagy, Nrf2 and astrocyte activation) in the brains of Old mice. Five-week daily supplementation with CLA (650 mg/kg-1 body weight) of 16-week old mice (CLA+Old) diminished all the pathological hallmarks at a level comparable to Y mice or healthy controls (BALB/c). Such data demonstrated that MRL/lpr mice can serve as a valuable model for the evaluation of the effectiveness of neuroprotective drugs. Notably, the preventive effect provided by CLA supplementation against age-associated neuronal damage and hyperactivation of compensatory mechanisms suggests that the activation of an adaptive response is, at least in part, accountable for its neuroprotective ability.

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