Brain’s own immune cells "infect" healthy neurons with Alzheimer-linked beta-amyloid protein. Digest
Alzheimer’s disease is a common neurodegenerative disorder affecting an estimated 24 million older adults worldwide. Researchers believe the disease is caused by toxic levels of beta-amyloid protein aggregates in the brain that impair neuronal function and trigger cognitive decline. While this process is partly under the influence of genes, studies also indicate links between Alzheimer’s and external factors such as head injury. Findings from a new study shed new light on this link, suggesting that events such as head trauma and stroke accelerate Alzheimer’s disease by activating one of the brain’s major immune cells and triggering an infection-like spread of amyloid-beta tangles to previously unaffected tissues.
The researchers conducted their experiments in mice genetically engineered to carry five mutations associated with Alzheimer’s disease. While these mutations lead to brain beta-amyloid aggregations and cognitive impairments at an early age, the team uncovered that even genetically healthy brain tissue could accumulate these aggregations if implanted into the brains of these mutant mice.
To better understand this infection-like phenomenon, the researchers examined whether the mutant brain cells of the host might import beta-amyloid particles by migrating into the transplanted tissue or making connections with its neurons. Tracking them under a microscope offered no support for this hypothesis. Instead, the team uncovered a mass migration into the implanted tissue of microglia, the main immune cells of the nervous system, specialized for scouting brain tissue for signs of injury or pathogen invasion and clearing out cellular debris.
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One possible reason for this migration is that microglia are drawn to wounds. Indeed, the microglia were particularly concentrated around the edges of the transplant and exhibited similar migrations to tiny brain lesions that the researchers generated using lasers. However, in moving from the genetically diseased to healthy tissue, the microglia dumped large numbers of beta-amyloid particles previously picked up from the degenerating host brain tissue.
The results offer an updated picture of Alzheimer’s disease progression where the brain’s own immune cells inadvertently drive the spread of pathogenic beta-amyloid aggregations – an effect that might be aggravated by brain injury events and inflammation. While scientists are uncertain why contaminated microglia engage in this “dumping” practice, targeting the cells' activity as a way of interfering with the neurodegenerative process provides promising research opportunities.