Differential Effects of Palmitoylethanolamide against Amyloid-β Induced Toxicity in Cortical Neuronal and Astrocytic Primary Cultures from Wild-Type and 3xTg-AD Mice

摘要: BACKGROUND Considering the heterogeneity of pathological changes occurring in Alzheimer's disease (AD), a therapeutic approach aimed both to neuroprotection and neuroinflammation reduction may prove effective. Palmitoylethanolamide (PEA) has attracted attention for its anti-inflammatory/neuroprotective properties observed AD animal models. OBJECTIVE AND METHODS We evaluated protective role PEA against amyloid-β₄₂ (Aβ₄₂) toxicity on cell viability glutamatergic transmission primary cultures cerebral cortex neurons astrocytes from triple-transgenic murine model (3xTg-AD) their wild-type littermates (non-Tg) mice. RESULTS Aβ₄₂ (0.5 μM; 24 h) affects cultured cortical non-Tg mice, but not those 3xTg-AD These effects were counteracted by pretreatment with (0.1 μM). Basal glutamate levels mice lower than cells Aβ₄₂-exposure reduced increased mouse astrocytes, respectively. PEA. By itself, did affect or CONCLUSION The exposure induced toxic Furthermore, exerts differential Aβ₄₂-induced In particular, displays neuronal overexpressing Aβ.