Our Brain’s Superhero Cells and Their Role in Alzheimer's Disease
If these cells had costumes, microglia would be draped in a superhero cape on constant patrol for bad guys.
Our Hero Microglia Cells and Alzheimer's Disease
Microglia cells do not mess around.
They live in and defend the brain and spinal cord against threats foreign and domestic, including, detecting damaged or unhealthy neurons. They eat the bad guys – or foreign invaders like bacteria and viruses – and display the chewed up parts on their cell surface to signal for help.
If these cells had costumes, they would be draped in a superhero cape on constant patrol for bad guys.
In the last few decades, scientists have focused on the role of the brain’s immune system in Alzheimer’s disease and in particular, these special immune cells called microglia.
Microglia are found only in the brain and comprise 10 to 15 percent of the cells of the brain. Microglia surround the amyloid plaques that Dr. Alois Alzheimer first identified as one of the hallmarks of this disease.
“More than 100 years ago, Alois Alzheimer sketched microglia cells that look rather similar to the modern images we have of these cells today,” says Jim Summers, Ph.D., vice president, neuroscience discovery research, AbbVie. “We know microglia cells are important. Yet scientists have been unable to determine their exact role in the cause and progression of this disease.”
Around 30% of the genes that have been discovered to either increase the risk or protect from Alzheimer's are associated with microglial functions. Microglia are also believed to play a role in the transmission of tau from neuron to neuron and in pruning synapses.
And yet, like most super heroes, microglia are not perfect and sometimes miss the mark. For reasons that aren’t understood, these microglia in some Alzheimer’s patients don’t clear the plaques as might be expected. Or maybe they do early in the Alzheimer's but simply can’t keep up and get overwhelmed as the disease progresses.
And so, scientists are particularly interested in genes expressed by microglia that have been linked to increased and decreased risk of Alzheimer such as CD33 and TREM2. They are also focused on the microglia that surround plaques to understand what ways are they different from other microglia and how might we encourage them to clear plaque.
“The road to find the cause and treatments to help Alzheimer’s patients has been a long, 100-plus year journey, making microglia a relatively new player on the research scene,” Summers says. “These cells may be only one piece to the story but their presence around amyloid plaques, their genetic association with disease, and their role in detecting damaged or unhealthy neurons make them worth studying.”