Role of inflammation and other immune responses in Alzheimer’s


Inflammation is the brain’s consistent fundamental response to trauma, whether the challenge is infection or injury. It also has emerged as a necessary component to the pathological cascade of Alzheimer’s, enabling amyloid aggregation and tau propagation to develop into clinically diagnosable disease. However, the roles of each protein—why they exist in the brain at all—and their interrelationship with inflammatory processes still are emerging.

Cure Alzheimer’s Fund is supporting efforts to investigate neuroinflammatory processes and feedback mechanisms as well as groundbreaking research uncovering a functional role for amyloid as an infection-fighting agent in the brain.

The laboratory of Rob Moir, Ph.D., recently advanced the novel idea that Abeta is part of the innate immune system and belongs to a family of proteins called antimicrobial peptides (AMPs). Unlike the responsive immune system, which creates antibodies and triggers inflammation, the innate immune system is evolutionarily very ancient and functions by providing an immediate response to pathogens. Because the brain does not have a responsive immune system generating pathogen-specific antibodies like the rest of the body, AMPs function as generic natural antibiotics to protect against invading pathogens. In vitro Abeta can inhibit the growth of at least eight clinically important pathogens. In addition, samples from the brains of AD patients have specific Abeta-mediated antimicrobial activity.

The discovery of Abeta’s role in innate immunity identifies pharmacological manipulation of the innate immune system as a new and promising therapeutic strategy for treating AD.