Hematopoietic MyD88-adaptor protein acts as a natural defense mechanism for cognitive deficits in Alzheimer's disease.

Accumulating evidence supports a critical role of Toll-like receptors in the clearance of Amyloid beta (Aβ) by microglial cells. Myeloid differentiation factor 88 (MyD88) is an adaptor protein that bridges the intracellular signal to nucleus for most of these innate immune receptors. We investigated here the role of competent MyD88 hematopoietic stem cells on the cognitive decline of a mouse model of Alzheimer's disease (AD).

MyD88-adaptor protein acts as a preventive mechanism for memory deficits in a mouse model of Alzheimer's disease.

Background: Alzheimer's disease (AD) is an age-related neurodegenerative disorder associated with brain innate immune activation mainly mediated by microglia. These cells are known to be activated in the brain of AD patients and to produce inflammatory cytokines and neurotoxic molecules in response to Amyloid beta (Aβ). Activation of microglia can also promote Aβ clearance via Toll-like receptors (TLRs).

Toll-like receptor 2 acts as a natural innate immune receptor to clear amyloid beta 1-42 and delay the cognitive decline in a mouse model of Alzheimer's disease.

Microglia are the immune cells of the brain, they are activated in the brain of Alzheimer's disease (AD) patients and mouse models of AD, and they express the innate immune receptor toll-like receptor 2 (TLR2). The present study investigated role of this receptor in the progression of AD-like pathologies. Here we show that amyloid beta (A beta) stimulates TLR2 expression in a small proportion of microglia.

In vivo functional genomics of Pseudomonas aeruginosa for high-throughput screening of new virulence factors and antibacterial targets.

Pseudomonas aeruginosa is a model for studying opportunistic pathogens that are highly resistant to most classes of antibiotics and cause chronic pulmonary infections. We have developed and adapted a multiplex polymerase chain reaction-based signature-tagged mutagenesis (STM) for high-throughput screening of a collection of 7968 P. aeruginosa mutants in a rat model of chronic respiratory infection.