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Evidence in animal models of CDD showed that absence of CDKL5 negatively affects neuronal survival, as well as neuronal maturation and dendritic outgrowth; however, knowledge of the substrates underlying these alterations is still limited. Neuroinflammatory processes are known to contribute to neuronal dysfunction and death. Recent evidence shows a subclinical chronic inflammatory status in plasma from CDD patients. However, to date, it is unknown whether a similar inflammatory status is present in the brain of CDD patients and, if so, whether this plays a causative or exacerbating role in the pathophysiology of CDD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We evaluated microglia activation using AIF-1 immunofluorescence, proinflammatory cytokine expression, and signaling in the brain of a mouse model of CDD, the\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mouse, which is characterized by an impaired survival of hippocampal neurons that worsens with age. Hippocampal neuron survival was determined by DCX, NeuN, and cleaved caspase-3 immunostaining in\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mice treated with luteolin (10 mg\/kg), a natural anti-inflammatory flavonoid. Since hippocampal neurons of\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mice exhibit increased susceptibility to excitotoxic stress, we evaluated neuronal survival in\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mice injected with NMDA (60 mg\/kg) after a 7-day treatment with luteolin.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found increased microglial activation in the brain of the\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mouse. We found alterations in microglial cell morphology and number, increased levels of AIF-1 and proinflammatory cytokines, and activation of STAT3 signaling. Remarkably, treatment with luteolin recovers microglia alterations as well as neuronal survival and maturation in\n                      <jats:italic>Cdkl5<\/jats:italic>\n                      KO mice, and prevents the increase in NMDA-induced cell death in the hippocampus.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results suggest that neuroinflammatory processes contribute to the pathogenesis of CDD and imply the potential usefulness of luteolin as a treatment option in CDD patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12974-021-02204-0","type":"journal-article","created":{"date-parts":[[2021,7,8]],"date-time":"2021-07-08T05:02:48Z","timestamp":1625720568000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Inhibition of microglia overactivation restores neuronal survival in a mouse model of CDKL5 deficiency disorder"],"prefix":"10.1186","volume":"18","author":[{"given":"Giuseppe","family":"Galvani","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola","family":"Mottolese","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Gennaccaro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuela","family":"Loi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giorgio","family":"Medici","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marianna","family":"Tassinari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Fuchs","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabetta","family":"Ciani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2623-2769","authenticated-orcid":false,"given":"Stefania","family":"Trazzi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,7,8]]},"reference":[{"issue":"3","key":"2204_CR1","doi-asserted-by":"publisher","first-page":"427","DOI":"10.1006\/geno.1998.5391","volume":"51","author":"E Montini","year":"1998","unstructured":"Montini E, Andolfi G, Caruso A, Buchner G, Walpole SM, Mariani M, et al. 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