Experimental Alzheimer’s Immunotherapy Shows Early Promise in Mice

Significant obstacles remain before potential human therapy.

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Immunotherapy could hold promising results for treating Alzheimer’s disease as well as other neurological disorders.

The therapy aims to harness the power of the immune system to remove harmful proteins in the brain associated with conditions like Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis (ALS), according to new study published in Science Translational Medicine.

Using Brain Cells to Target Plaques and Tangles

Typically used for cancer treatment, immunotherapy works by harnessing the body’s immune system to recognize and attack harmful cells.

In the context of neurological diseases, immunotherapy uses the brain’s immune cells, known as microglia, to target the amyloid beta plaques associated with Alzheimer’s disease.

As these plaques build up in the brain, another protein called tau also forms and becomes entangled with neurons, ushering in the second stage of Alzheimer’s characterized by brain atrophy and cognitive decline.

While the precise role of these plaques and tangles in Alzheimer’s is not fully understood, the scientific consensus is that they play a vital part in disrupting communication between nerve cells and interfering with essential cellular processes, according to the Alzheimer’s Association.

Immune Cells Contain Plaques, But Antibodies Clear Them

Researchers tested the immunotherapy approach on mice. They found that when activated, the brain’s immune cells will surround the amyloid beta plaques and form a protective barrier. This barrier prevents the plaques from spreading further.

The microglia’s inability to fully destroy the plaques, which is typically the goal of immunotherapy, is neutralized by a component of the plaques themselves.

However, the research team found that specially engineered antibodies were able to successfully block and clear the plaques. Clearing these plaques in the mice was found to alleviate their risk-taking behaviors often observed in Alzheimer’s.

“By activating microglia generally, our antibody can remove amyloid beta plaques in mice, and it could potentially clear other damaging proteins in other neurodegenerative diseases, including Parkinson’s disease,” Dr. Marco Colonna, the study’s senior author, said in a press release.

Search for Better Treatments Continues

Dr. Colonna and his team believe that their immunotherapy approach could alter the later stages of Alzheimer’s disease. They theorize that by clearing the amyloid beta plaques, it may prevent or slow the formation of the tau protein tangles. However, this hypothesis will require additional research and testing specifically focused on the tau tangles.

Current Alzheimer’s drug treatments have limitations. Medications like lecanemab, which target the amyloid proteins, can sometimes induce side effects like swelling and bleeding (a condition known as ARIA).

While lecanemab has been approved by the FDA to treat the condition, it is not a cure and is considered the “first traditionally approved treatment that addresses the underlying biology of Alzheimer’s and changes the course of the disease in a meaningful way for people in the early stages,” according to the Alzheimer’s Association.

“Lecanemab, as the first therapeutic antibody that has been able to modify the course of the disease, confirmed the importance of amyloid beta protein in Alzheimer’s disease progressionaccording to the study authors. ”And it opened new opportunities for developing other immunotherapies that use different methods of removing damaging proteins from the brain.”

The approval of lecanemab confirmed the critical role of the amyloid beta protein in the progression of the condition, the study authors noted. The medication opened up new avenues for developing other immunotherapy approaches that uses different methods to remove harmful proteins from the brain, they added.