Alzheimer's disease, as well as other neurodegenerative disorders are characterized by damage to brain tissue. Immune cells within the brain participate in disease progression, whether by slowing it down or escalating disorders severity. Microglia are immune cells that reside within the central nervous system (CNS) and participate in immune activity, particularly phagocytosis. As such, microglia can either contribute to or inhibit Alzheimer's progression, and manipulating them may provide a unique therapeutic option to treat Alzheimer's and other CNS-related disorders.
The groups of Profs. Ido Amit and Michal Schwartz used innovative single cell sequencing technologies in order to characterize these microglias and consequently discovered a series of potential immune checkpoints. Therefore, modulating these checkpoint targets could be a treatment for Alzheimer's disease and other diseases that are related to microglia dysfunction.
The Amit and Schwartz groups widely characterized DAMs by single-cell sequencing techniques and found a number of molecules that participate in their immune function. These DAMs were found not only in brains of mouse Alzheimer's model, but also in brains of humans with Alzheimer's that were analyzed post-mortem. The group also expanded the research to other neurodegenerative diseases in mice models, and confirmed DAM presence in these models as well. Therefore, these DAM regulatory molecules hold potential as treatment for a number of neurodegenerative.