Lijun Ni

Juvenile influenza can impair myelin development and adult behavior through chemokine signaling in mice

This study shows that juvenile influenza infection in mice impairs myelin development and leads to lasting cognitive and behavioral issues, which can be mitigated by inhibiting the chemokine receptor CCR3.

Immunotherapy-related cognitive impairment after CAR T cell therapy in mice

This study shows that CAR T cell therapy in mice causes cognitive impairment through CNS immune dysregulation, microglial reactivity, and disrupted oligodendroglial homeostasis.

GABAergic neuron-to-glioma synapses in diffuse midline gliomas

This study identifies functional GABAergic neuron-to-glioma synapses in diffuse midline gliomas that promote tumor proliferation and shows that drugs modulating GABAergic signaling affect glioma growth.

Myelin plasticity in ventral tegmental area is required for opioid reward

The paper shows that myelin plasticity in the ventral tegmental area, regulated by dopaminergic activity, is essential for opioid reward and dopamine release dynamics.

Glioma synapses recruit mechanisms of adaptive plasticity

This study shows that BDNF-TrkB signaling promotes malignant synaptic plasticity in gliomas, enhancing tumor progression through mechanisms similar to long-term potentiation in the healthy brain.

Epigenetic neural glioblastoma enhances synaptic integration and predicts therapeutic vulnerability

The paper identifies an epigenetic neural signature in glioblastoma that correlates with poor prognosis and therapeutic vulnerability.

Mild respiratory SARS-CoV-2 infection can cause multi-lineage cellular dysregulation and myelin loss in the brain

Respiratory-restricted SARS-CoV-2 infection in mice, without brain virus, drives white matter microglial reactivity, impaired neurogenesis, oligodendrocyte depletion and myelin loss lasting at least 7 weeks.

Maladaptive myelination promotes epileptogenesis in absence epilepsy

This study shows that maladaptive myelination driven by absence seizures contributes to epileptogenesis in two mouse models of absence epilepsy.