Currently, 32 million people live with Alzheimer’s disease around the world. With a growing aging population, Alzheimer’s, a form of dementia, might spike to 152 million by 2050. Right now, there is no cure for Alzheimer’s disease, and medication options are limited. Therefore, researchers are focused on finding ways to treat this type of dementia.
Scientists have been exploring immunotherapy, a treatment that boosts the body’s immune response to fight Alzheimer’s disease. A potential treatment area scientists have been exploring is immunotherapy, which is a treatment that boosts the body’s immune response — to fight Alzheimer’s disease. According to a study by Science Translational Medicine, researchers showcase a way to use antibodies to restore the nervous system’s immune cells’ ability to clear out unwanted debris that may lead to Alzheimer’s disease.
Specific monoclonal antibodies, like lecanemab and aducanumab, have been approved by the FDA [Food and Drug Administration] for Alzheimer’s treatment. Other monoclonal antibodies enhance microglial responses to amyloid-beta pathology by activating the TREM2 receptor and are undergoing clinical trials.
Researchers use a mouse model to test their strategy, which focuses on targeting proteins that regulate the activity of microglia, a type of immune cell in the nervous system. Microglia respond to signals from the tissue environment, activating and inhibitory. Their primary role is to clear toxic substances that build up within the brain by phagocytosis. These toxins send signals, prompting microglia to engulf them.
The microglia must also safeguard the brain’s healthy components, which send signals to deter microglial activity. Researchers can provide activating stimuli or block inhibitory ones to enhance microglial phagocytic function. The strategy focuses on inhibiting receptors that dampen microglial phagocytosis.
Past studies have suggested that microglia may help combat neuroinflammation and clear out the toxic accumulation of proteins like tau and beta-amyloid associated with Alzheimer’s disease.
The team of researchers also studied the impact of the LILRB4 receptor, located on the microglia in the brain, and how it may impact the development of Alzheimer’s disease.LILRB4 is a receptor found on brain microglia, and it interacts with a fat-carrying protein called ApoE, which is abundant in the brain and is also a part of amyloid plaques associated with Alzheimer’s disease.
Researchers discovered high amounts of LILRB4 on microglial surfaces in brain tissue samples from people with Alzheimer’s. The scientists then used a mouse model capable of expressing the human LILRB4 receptor. Their experiments showed that the LILRB4 receptor disrupted the microglia’s ability to interact with beta-amyloid plaques.
Treating the mice with antibodies against LILRB4 resulted in lower beta-amyloid amounts in the brain and increased microglial activity. It reversed some behavioral changes during maze tests that the scientists had linked to beta-amyloid accumulation.
Based on the recent findings, researchers think treating Alzheimer’s with a specific monoclonal antibody can help the brain clear amyloid plaques and other harmful proteins that build up in neurodegenerative diseases. This study is just a possibility of the impact of such protective functions within the etiology of Alzheimer’s. Research on effective treatment for Alzheimer’s is still required.
