Previous research looking into the underlying causes of Alzheimer’s disease have focused on the accumulation of a protein known as amyloid-beta. In a new study, however, a team of researchers from the University of Chicago examined the role of neurogenesis in genetic forms of the neurodegenerative disease.
In the study, as published in the Journal of Neuroscience, the team looked at presenilin 1 and presenilin 2, mutations in two genes known to cause early onset of Alzheimer’s. In past studies on rodents with mutations of both genes, it was determined that when placed in an enriched environment, there was no significant increase in brain cells and instead, the rodents exhibited traits of anxiety, a hallmark symptom during the early stages of the neurodegenerative disease.
Researchers focused on microglia, which acts as an active immune defense in the central nervous system. Microglia removes excessive levels of amyloid beta, eliminates dying cells, and repairs synapses. Neurogenesis was restored to normal upon administering a substance to the rodents utilized for microglial cell death. Among the rodents with presenilin mutations, they showed no signs of memory decline or anxiety when placed into an enriched environment.
“Once you wipe out the microglia, all these deficits that you see in these mice with the mutations are completely restored. You get rid of one cell type, and everything is back to normal,” said Sangram Sisodia, lead researcher of the study. “It’s the most astounding result to me.”
“This is another way to understand the biology of these genes that we know significantly affect the progression of disease and loss of memory.”