Alzheimer’s disease (AD) has a new candidate for its treatment. Nasal anti-CD3 monoclonal antibody (MAb) reduced microglia activation in the brain of mice without its effect being dependent on the β-amyloid (Aβ) deposits characteristic of this neurodegenerative disorder. “We have done many basic studies in the laboratory on microglia. Microglia activation occurs in many neurologic diseases. One of them is multiple sclerosis (MS). And it also occurs in AD,” senior author Howard Weiner told BioWorld.
In brain research, be it basic or clinical, neurons have long hogged the limelight. But at the 2023 European Meeting on Glial Cells in Health and Disease, neurons take a back seat to glia – cell types that have often been described as support cells and treated as an afterthought, but that play critical roles in all aspects of brain function, including information processing.
“One of the many reasons we don’t have effective therapies for AD at the moment ... is that we don’t understand the beginnings of the disease,” Constanze Depp told BioWorld. Understanding those beginnings is likely to be a necessary prerequisite for truly turning the tide on Alzheimer’s disease (AD). “The brain is so bad at repairing itself, and once a neuron is lost, it will most likely not regenerate,” she elaborated. Now, Depp and her colleagues have reported on a contributor to those beginnings.
While microglia constitute the immune cells of the brain, their potential role in the early development of neuronal circuitry is poorly understood. Investigators at the Karolinska Institutet, together with eight other institutions, characterized an anatomically distinct microglial cell population identified as expressing the arginase-1 (ARG1) enzyme.
Implanting brain organoids into the brains of mice may allow the more realistic study of microglial cells during both healthy and disease states. This is what researchers from the Salk Institute and their collaborators found in a study published on May 11, 2023, in Cell.
Research shows that microglia, macrophage cells found in the central nervous system, are needed to maintain nerve health by preventing the degeneration of the myelin sheath that protects neurons. The study, led by the University of Edinburgh and the University of Toronto and published on Dec. 14, 2022, in Nature, showed microglia could be a potential therapeutic target for neurological conditions involving myelin degeneration.
Tyrosine kinase SYK (spleen tyrosine kinase), an enzyme involved in immune signaling, could play a key role in Alzheimer's disease (AD), multiple sclerosis (MS), and other neurodegenerative diseases, according to a study from the University of Virginia (UVA). SYK regulates the activity of microglia, preventing the accumulation of secretions associated with AD or MS produced in these pathologies.
As the resident innate immune cells of the brain, microglia are emerging as key drivers of neurological diseases, but as yet there is no systematic way of exploring their potential as drug targets.
Researchers at Stanford University have developed a method to efficiently replace microglia, which are brain-specific immune cells, via a modified bone marrow transplant.
Researchers at Stanford University have developed a method to efficiently replace microglia, which are brain-specific immune cells, via a modified bone marrow transplant.
