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Boda, E.

Publications and source records attributed to Boda, E..

2 recordsLinked to original sources

Acute particulate matter (PM10) exposure selectively triggers behavioral alterations in the presymptomatic Experimental Autoimmune Encephalomyelitis (EAE) mouse model of Multiple Sclerosis

Multiple Sclerosis (MS) is a chronic disease of the Central Nervous System, where neuroinflammation and autoimmune response against myelin lead to functional impairments, cognitive and psychiatric symptoms. Exposure to air pollution - in particular to peaks of particulate matter (PM) - has been associated with an increase of hospital admissions for MS onset and relapses and exacerbated neuroinflammation in MS patients. Here, in the MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) mouse model of MS, we tested the hypothesis that exposure to PM10 might influence the disease course and severity in individuals with a predisposing background. Short-term PM10 exposures - occurring either before immunization or during the pre-symptomatic phase - did not modify disease manifestation in EAE mice, as assessed by clinical and neuropathological analyses. Yet, presymptomatic EAE - but not healthy - mice selectively showed increased disinhibited, risk-taking and novelty-seeking behaviors early after being exposed to PM10. These data show a selective vulnerability of immunologically primed mice toward the effects of PM10, occurring before the emergence of overt motor impairment and presenting as specific behavioral alterations.

neuroscience↗

Mecp2 knock-out astrocytes affect synaptogenesis by IL-6 dependent mechanisms

Synaptic abnormalities represent a hallmark for several neurological diseases and clarification of the underlying mechanisms constitutes a crucial step towards the development of therapeutic strategies. Rett syndrome (RTT) is a rare neurodevelopmental disorder, mainly affecting females, caused by heterozygous mutations in the X-linked Methyl-CpG-Binding Protein 2 (MECP2) gene, leading to a deep derangement of synaptic connectivity. Although initial studies have supported the exclusive involvement of neurons, recent data have highlighted the pivotal contribution of astrocytes in RTT pathogenesis through non-cell autonomous mechanisms. Since astrocytes regulate synaptogenesis by releasing multiple molecules, we investigated the influence of soluble factors secreted by Mecp2 KO astrocytes on synaptic density. We found that Mecp2 deficiency in astrocytes negatively affects their ability to support synapse formation by releasing synaptotoxic molecules, among which we identified interleukin-6 (IL-6). Notably, aberrant IL-6 expression exclusively emerges from a dysfunctional astrocyte-neuron crosstalk, and blocking IL-6 activity prevents synaptic alterations.

neuroscience↗