Stanford’s latest research, published in the Journal of Clinical Investigation, shows success in staving off memory loss and other symptoms associated with Alzheimer’s disease in mice. Led by Stanford neuroscientist Katrin Andreasson, MD, the research team reactivated microglial cells by blocking a receptor on the cell called EP2, leading to improvements in mice predisposed to Alzheimer’s.

Microglial cells are a type of brain cell that act as the first line of immune defense and clean out the protein Amyloid beta (A-beta). If A-beta is not cleared out, it can build up into amyloid plaques, which are found in individuals afflicted with Alzheimer’s disease. During the aging process, microglial cells gradually stop working, leading to the A-beta’s build-up.

Through genetic manipulation, Dr. Andreasson and her team were able to block the activity of EP2, a receptor protein on the surface of the microglial cell, so that the microglia could return to normal functioning. Deactivating the EP2 receptor led to restoration of the microglial response to A-beta build-up; the cell resumed cleaning up the protein and suppressed toxic neuroinflammation. Blocking of the EP2 receptor also led to the promotion of IGF1, an insulin-like growth factor that is neuroprotective, anti-inflammatory, and able to enhance plasticity in the brain, boosting cognitive functioning.

Simply put, the microglia returned to their prior level of functioning, clearing out A-beta, reducing inflammation in the brain and preventing build-up of amyloid plaques. This process prevented memory deficits and synaptic injuries, meaning that the neural, chemical and electrical signals between neurons were able to function normally. Researchers also found that the mice in the study improved on a multitude of memory tests, and their IQs increased.

Though targeting microglia may not be a cure-all, this discovery is a huge step in the right direction. Clearing out the build-up of A-beta and enhancing the immune defense of the brain are two critical components of preventing or delaying Alzheimer’s. We are looking forward to further breakthroughs from top research facilities, such as Stanford, in Alzheimer’s and dementia research.

Sources

Goldman, Bruce. “Blocking Receptor in Brain’s Immune Cells Counters Alzheimer’s in Mice, Study Finds.” News Center. Stanford Medicine, n.d. Web.

Goldman, Bruce. “Blocking a Receptor on Brain’s Immune Cells Counters Alzheimer’s in Mice.” Scope Blog RSS. Stanford Medicine, n.d. Web.

“Insulin-like Growth Factor 1.” Wikipedia. Wikimedia Foundation, n.d. Web.

“Prostaglandin Signaling Suppresses Beneficial Microglial Function in Alzheimer’s Disease Models.” The Journal of Clinical Investigation. N.p., n.d. Web.