Complement is involved in developmental synaptic pruning and pathological synapse loss
in Alzheimer's disease. It is posited that C1 binding initiates complement activation on …

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 …

Complement pathway overactivation can lead to neuronal damage in various neurological
diseases. Although Alzheimer's disease (AD) is characterized by β-amyloid plaques and tau …

The complement system is increasingly recognized as a key player in the synapse loss and
cognitive impairments observed in Alzheimer's disease (AD). In particular, the process of …

The complement system is implicated in synapse loss in the MS hippocampus, but the
functional consequences of synapse loss remain poorly understood. Here, in post-mortem …

Alzheimer's disease (AD) is a neurodegenerative disease resulting in progressive cognitive
decline. Amyloid plaque deposits consisting specifically of β‐amyloid peptides that have …

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 …

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

Background Complement proteins and activation products have been found associated with
neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was …