Shirin Hosseini

TL;DR: Evidence is provided that neuroinflammation induced by neurotropic H7N7 and infection of the lung with a non-neurotropic H3N2 IAV result in long-term impairments in the CNS, indicating that IAV-associated inflammation induced functional and structural alterations in hippocampal networks.

TL;DR: It is suggested that 3 mo of OLT1177 diet can rescue synaptic plasticity in this mouse model of AD and the therapeutic potential of treating neuroinflammation with an oral inhibitor of the NLRP3 inflammasome is suggested.

TL;DR: In the hippocampus of healthy IFNAR-deficient mice, synapse number and synaptic plasticity, as well as spatial learning, are impaired, and levels of the astrocytic glutamate-aspartate transporter (GLAST) are reduced significantly upon IFN-β treatment and increase following inhibition ofIFNAR signaling.

TL;DR: In this article, the role of purely peripheral IAV infection for the development and progression of Alzheimer's disease in a transgenic mouse model (APP/PS1) was investigated.

TL;DR: It is demonstrated that subclinical infections by viruses from the TBEV-serogroup affected anxiety-like behavior and induced far-reaching effects on hippocampal neuron morphology and impaired hippocampus-dependent learning and memory formation.