Complement overactivation mediates microglial synapse elimination in neurological
diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how …

Recent discoveries implicate the classical complement cascade in normal brain
development and in disease. Complement proteins C1q, C3, and C4 participate in synapse …

Systemic inflammatory reactions have been postulated to exacerbate neurodegenerative
diseases via microglial activation. We now demonstrate in vivo that repeated systemic …

Cortical pathology contributes to chronic cognitive impairment of patients suffering from the
neuroinflammatory disease multiple sclerosis (MS). How such gray matter inflammation …

Microglia survey the brain microenvironment for signals of injury or infection and are
essential for the initiation and resolution of pathogen‐or tissue damage‐induced …

Amyloid plaques, mainly composed of abnormally aggregated amyloid β-protein (Aβ) in the
brain parenchyma, and neurofibrillary tangles (NFTs), consisting of hyperphosphorylated tau …

The complement inhibitor, Crry, which blocks both the classical and alternative pathways,
alleviates CNS disease in the lupus model, MRL/MpJ‐Tnfrsf6lpr (MRL/lpr) mice. To …

Elements of the immune system particularly that of innate immunity, play important roles
beyond their traditional tasks in host defense, including manifold roles in the nervous …

Previous studies demonstrate that activation of pancreatic ER kinase (PERK) protects
oligodendrocytes against inflammation in the experimental autoimmune encephalomyelitis …

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology.
Neuropsychiatric disturbances unexplained by drugs or by other untoward manifestations of …