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Astrocytes from ALS patients release inflammatory molecules instead of providing energy support, which is often responsible for microglia shifting to an inflammatory state incurring neuronal damage (Table 2)

Although these genes are components of the hyperinflammation caused by SARS-CoV-2 ( IL6 and IL17A in patients with COVID-19 ( CCL3 and IL1B stand out, both with a central role in the pathophysiology of COVID-19 and highly expressed in peripheral blood mononuclear cells during the disease ( CCL3 expression is higher in COVID-19 patients with an unfavorable outcome ( The transcriptional signatures observed at endpoint Z remained for the most part conserved after incubation of cultures for 24h (endpoint A), thus validating the ex vivo model of whole blood cultures for researching drugs with the potential to fight hyperinflammation in COVID-19

Trends Plant Sci 26(6):560574

Clayton LW

Abstract As global life expectancy increases, research reveals a critical challenge in aging: the progressive deterioration of immune function, termed immunosenescence