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 …

C1q, a member of the immune complement cascade, is implicated in the selective pruning of
synapses by microglial phagocytosis. C1q-mediated synapse elimination has been shown …

In mature neurons, the number of synapses is determined by a neuronal activity-dependent
dynamic equilibrium between positive and negative regulatory factors. We hypothesized that …

Accumulation of amyloid-β (Aβ) is thought to play a central role in the progressive loss of
synapses, the neurite damage, and the neuronal death that are characteristic in brains …

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

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

Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid
(Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD) …

C1q, the recognition component of the classical complement activation pathway, is a
multifunctional protein of the immune system that has been shown to be expressed in the …

Synapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is
currently the best correlate to cognitive decline. Microglial cells are involved in synapse …

The innate immune system plays an integral role in the brain. Synaptic pruning, a
fundamental process in developmental circuit refinement, is partially mediated by …