Can we leverage immunotherapy against Alzheimer’s disease?

Can we leverage immunotherapy against Alzheimer’s disease?

The most prevalent type of dementia, Alzheimer’s disease, affects approximately 32 million people worldwide. Experts predict that the number of dementia cases will rise to 152 million by 2050 due to an aging population. Alzheimer’s disease currently has no known treatment options and no cure. Because of this, scientists have been working to develop new treatments for this kind of dementia. Immunotherapy, a treatment that strengthens the body’s immune response to combat Alzheimer’s disease, is one possible avenue of treatment that researchers are investigating.

The journal Science Translational Medicine published one of the most recent studies on immunotherapy for Alzheimer’s disease. Researchers from Washington University in St. Louis conducted this study. Louis describes how to use antibodies to help the immune cells in the nervous system remove unnecessary debris that can cause Alzheimer’s disease. Alzheimer’s disease currently has no known cure and current treatments only provide symptomatic relief.

The FDA [Food and Drug Administration] has approved lecanemab and aducanumab, two monoclonal antibodies, for treating Alzheimer’s disease. Clinical trials are being conducted on other monoclonal antibodies that activate the TREM2 receptor, thereby improving microglial responses to amyloid-beta pathology. However, more research is needed to determine how effective these treatments are. To improve overall efficacy, it is imperative to investigate alternative approaches that may prove to be more efficacious or serve as a supplement to currently available monoclonal antibody treatments.

The researchers used a mouse model to test their approach, which focused on proteins that control the activity of a particular type of immune cell in the nervous system called microglia. According to Colonna, microglia react to both activating and inhibitory cues from the surrounding tissue. Their main function is to eliminate poisonous substances that accumulate in the brain through phagocytosis, a process in which cells “consume” foreign substances. The signals that these toxins send cause microglia to engulf them.

The healthy components of the brain, which send signals to inhibit microglial activity, must be protected at the same time by microglia, he continued. Blocking inhibitory stimuli or supplying activating ones will both improve microglial phagocytic function. Receptors that reduce microglial phagocytosis are the main target of our strategy. Microglia may be able to reduce neuroinflammation and remove the harmful buildup of proteins like tau and beta-amyloid, which are linked to Alzheimer’s disease, according to earlier research.

Colonna and his colleagues also investigated the potential role of the brain microglia-resident LILRB4 receptorTrusted Source in the pathogenesis of Alzheimer’s disease. Brain microglia contain the receptor LILRB4, which binds to ApoETrusted Source, a fat-transporting protein that is both widely distributed in the brain and a component of amyloid plaques linked to Alzheimer’s disease. Alzheimer’s disease risk is elevated in certain human population variants of [the gene that expresses] ApoE. High levels of LILRB4 were first found on microglial surfaces in brain tissue samples from Alzheimer’s patients, according to research.

A mouse model that could express the human LILRB4 receptor was then employed by the scientists. It was demonstrated by their experiments that the microglia’s interaction with beta-amyloid plaques was interfered with by the LILRB4 receptor. Beta-amyloid accumulation in the brain was linked to behavioral changes in maze tests, but treatment with antibodies against LILRB4 resulted in decreased beta-amyloid levels in the brain and increased microglial activity.

We found that the ability of microglia to remove amyloid plaques is slowed down when ApoE binds to LILRB4, as Colonna explained. The capacity of microglia to remove these plaques is, however, increased when a particular antibody is used to prevent ApoE from attaching to LILRB4. This implies the possibility of amyloid plaque removal from Alzheimer’s patients treated with this antibody. Based on these results, we believe that administering this particular monoclonal antibody to patients with Alzheimer’s disease may aid in the brain’s removal of amyloid plaques and other toxic proteins that accumulate in neuron diseases. To improve the efficacy of other currently being tested treatments, this one may also be combined with them.

This study offers more proof of the potential of neuroimmunologyTrusted Source to treat and, eventually, cure Alzheimer’s disease, according to a board-certified neuropsychologist who was not involved in the research and who reviewed it for MNT. More evidence that monoclonal antibodies can disrupt the accumulation of beta-amyloid, one of the main disease biomarkers, comes from these research findings. She pointed out that we still don’t know how protection against cognitive decline and the progression of the disease is provided by reducing amyloid from this novel mechanism, anti-LILRB4 microglia signaling.

According to Sullivan, there will be a dramatic increase in the number of people with dementia as a result of the so-called “graying of the world.”. We must direct all available resources toward the treatment and medical management of these diseases because the substantial rise in the number of cases of neurodegenerative disorders has a huge financial and psychological cost. Toxins and other hazardous substances are kept out of the brain by the brain-protecting blood-brain barrier, which is maintained in part by microglia. This study outlines the potential consequences of disrupting these protective functions in the etiology (also known as the causal mechanisms) of Alzheimer’s disease, as well as potential treatments.

Effective Alzheimer’s disease treatment is still a goal of ours. One potential course of treatment would be to restore microglia function. The most prevalent type of dementia, affecting millions of people globally, is Alzheimer’s disease. Because of aging populations, it is anticipated that the number of cases will rise dramatically in the ensuing decades. It is a global public health emergency because it significantly increases the financial and caregiving load on families, communities, and society as a whole. According to the expert, there is currently no effective treatment that can halt or reverse the course of the disease. She continued, Our ongoing research suggests that multiple processes/risk factors may be involved in the development of Alzheimer’s disease. Investigating different therapies that can halt or slow down the neurodegenerative process is therefore crucial.


Medications that have been suggested by doctors worldwide are available here

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