In a recent study, the Rutgers team found clearer evidence of how Alzheimer’s-linked destructive proteins attack human brain cells and destroy surrounding tissue.
There is no cure for Alzheimer’s, which is why Rutgers scientists are examining human brain cells in mice to identify a pivotal mechanism that could result in a potential therapy for the disease.
More on Alzheimer’s
In California, 690,000 people aged 65 and older are living with Alzheimer’s, a degenerative brain disease and the most common form of dementia.
In the United States, 5.8 million people aged 65 and older live with Alzheimer’s disease. Alzheimer’s affects memory, thinking, and behavior, and symptoms eventually grow in severity to interfere with daily tasks.
More on the study
Researchers at Rutgers injected human brain immune cells into the brains of specially bred immunodeficient mice, creating what they call a human‑mouse chimera. They then examined how microglia—specialized immune cells in the brain—responded after exposure to tau proteins, which are implicated in Alzheimer’s and other severe neurological diseases.
“This provided an unprecedented opportunity to study human microglia in the brain and the cognitive impairment seen in Alzheimer’s disease and Down syndrome,” said Peng Jiang, associate professor of Cell Biology and Neuroscience at Rutgers.
The mechanism of Alzheimer’s
Using this chimeric model—which allows human cells to grow, develop, and function normally—the scientists observed a cellular attack that has largely been hidden until now. In autopsies, researchers can examine brains from people who died with Alzheimer’s and see tau deposits and cell changes. But the chimera let the Rutgers team extract and analyze human cells during the degenerative process.
The mice were bred to be immunodeficient so they could accept human cells without rejection. Researchers injected them with human microglia, then later with tau proteins linked to Alzheimer’s.
“Since microglial cells are among the first responders when something goes wrong in the brain, we believe the changes we saw are significant,” said Mengmeng Jin, a postdoctoral researcher and first author on the study.
The California Institute for Regenerative Medicine is committed to investing at least $1.5 billion in treatments for conditions affecting the brain and central nervous system—including Alzheimer’s—more than double what CIRM invested between 2006 and 2020.
Read the source release here.
Mice and humans have evolutionary conserved brains meaning they have very similar brain architecture made up of similar types of brain cells. Hence, mice are idea subjects for neuroscientis who don’t have the ability to peer into living human brain. Microglial cells are the most prominent immune cells of the CNS. They are first to respond when something goes wrong in the brain. They regulate brain development primary through 2 routes : the release of diffusible factors and phagocytosis. Brain of human and mice do not proses similar types of antigen presentation molecules. It is interesting to investigate the molecular markers interplay to have prolong effect and cripple of microglial function. Evidence established that IFNAR endocytisis as an active contributor to the regulation of signal tranduction trigger by IFN binding to the IFNAR. However, DS microglial exhibit an enhanced synaptic pruning function, cellular senescent and elevated type 1 interferon signaling. Therefore, the determination of downstream regulator play roles to develop defective microglial from oversignaling of type 1 interferon may provide important insight of treatment for brain diseases.