Alzheimer’s disease affects around 32 million people globally, a number expected to increase in the next 25 years. As of now, there is no cure for Alzheimer’s disease, and the available medication options are limited. One potential treatment area that scientists have been exploring is immunotherapy, which aims to boost the body’s immune response to fight the disease. Researchers from Washington University in St. Louis have developed a new strategy that utilizes antibodies to restore the nervous system’s immune cells’ ability to clear out unwanted debris that may lead to Alzheimer’s disease.
The study focused on targeting proteins that regulate the activity of microglia, a type of immune cell in the nervous system. Microglia play a crucial role in clearing out toxic substances in the brain by phagocytosis, a process where the cells ‘consume’ foreign substances. By inhibiting receptors that dampen microglial function, researchers aimed to enhance the cells’ ability to clear out toxic proteins associated with Alzheimer’s disease. The LILRB4 receptor, found on brain microglia, interacts with a protein called ApoE, which is abundant in the brain and part of amyloid plaques linked to Alzheimer’s.
Using a mouse model expressing the human LILRB4 receptor, the researchers found that treating the mice with antibodies against LILRB4 resulted in decreased beta-amyloid levels in the brain, increased microglia activity, and reversed some behavioral changes associated with the accumulation of toxic proteins. The study suggests that blocking the interaction between ApoE and LILRB4 could help enhance the brain’s ability to clear out amyloid plaques. This specific monoclonal antibody treatment could potentially be used in combination with existing treatments to improve efficacy.
Neuropsychologist Karen D. Sullivan and geriatric specialist Manisha Parulekar, who were not involved in the study, highlighted the importance of research in neuroimmunology for treating and potentially curing Alzheimer’s disease. Sullivan emphasized the significance of monoclonal antibodies in interfering with the build-up of beta-amyloid, a key biomarker of the disease. However, questions remain about how reducing amyloid levels through this new mechanism may impact cognition and disease progression. Parulekar pointed out that the increasing number of dementia cases worldwide poses a significant public health crisis, necessitating effective treatments to slow down or stop the neurodegenerative process.
The study conducted by Washington University researchers provides insights into the potential of immunotherapy in treating Alzheimer’s disease by targeting microglial function. The findings suggest that blocking the interaction between ApoE and LILRB4 could help enhance the brain’s ability to clear out toxic proteins associated with the disease. Further research is needed to understand the cognitive benefits of reducing amyloid levels through this new mechanism and how it may impact the course of the disease. With the growing number of dementia cases globally, effective treatments are urgently needed to alleviate the financial and caregiver burden on individuals, families, and society.
