Scientists Have Discovered An Immune Cell That May Partially Reverse Damage Caused by ALS and MS

A series of articles recently published in FierceBiotech describe a discovery by Ohio State and Michigan University scientists. The teams have discovered an immune cell that could be tapped to partially reverse damage caused by neurodegenerative disorders.

Until now, the damage to nerve fibers caused by disorders such as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) could not be reversed. The scientists believe that the newly discovered immune cell may also slow the progression of these disorders.

Discovering Granulocytes

The researchers studied mouse models and found a type of white blood cell called granulocyte that resembles an infection-fighting neutrophil (a white blood cell).

The granulocyte secretes growth factors that regulate cell division and cell survival. They help the central nervous system axons to regenerate. The axon is a nerve cell (neuron) that directs nerve impulses away from the cell body.

“Really Unprecedented”

Dr. Benjamin Segal, Ohio State neurology chair, commented that the granulocyte subset’s ability to stimulate nerve fiber regrowth is “really unprecedented”.

He predicted that continuing this research will lead to creating cell-based therapies that will be able to restore neurological functions in many different disorders.

A Regrowth in Fibers

The research team found that the granulocytes had similar characteristics to immature neutrophils. They ran tests using mouse models and injected the recently discovered granulocytes into the mice that had either an injury to optic nerves or damaged nerve fibers.

The nerve fibers had regrown in the mice that were injected with the granulocytes, while the mice that were injected with mature neutrophils showed no fiber regrowth.

Slowly Coming Together

Neurological researchers have speculated for years that solutions to brain diseases might be found in immunotherapy.

In 2019 researchers at Stanford University identified a subset of CD8 T cells. When a peptide (a molecule containing amino acids) was used to boost the CD8 T cells in laboratory mice, their MS symptoms were greatly reduced.

An encouraging report by Mount Sinai’s Medical School last month stated that microglia (immune cells) can control neuron activity in various disorders such as Huntington’s and Alzheimer’s.

For years scientists were of the opinion that neurons generally kept the activity circuit in balance. But recently, a team of researchers directed by officials at the Icahn Medical School at Mount Sinai attributed the regulation of behavior in part to immune cells (microglia) in the brain.

Microglia remove cells that are dying. They are considered scavengers. A team at Stanford University found that a B-cell receptor called CD22 contributes to an age-related decline in microglia’s ability to clean up the central nervous system’s toxic debris.

When they reduced the levels of CD22, the cognitive function in the aged mice improved.

In one of the newest studies the team confirmed that just like inhibitory neurons, microglia are able to suppress surplus neuronal activation.

Ready for the Second Level

Both Ohio State and Michigan University researchers are ready to move to the next level. They must not only collect the neuro-enhancing granulocytes but must decide how to amplify them in the laboratory.

This should lead the researchers to not only treat ALS and MS, but to accomplish their goal of treating damage to the spine and the brain.

Another player in the development of drugs that treat neurodegenerative diseases that target microglia dysfunction is a startup company named Tranquis Therapeutics. Tranquis has already accumulated animal data in Parkinson’s, ALS, dementia, and neuropathologies.

Researchers are aware of the long journey ahead but they are committed to continuing their work involving immune cells and how they assist in the treatment of neurodegenerative disorders.

Rose Duesterwald

Rose Duesterwald

Rose became acquainted with Patient Worthy after her husband was diagnosed with Acute Myeloid Leukemia (AML) six years ago. During this period of partial remission, Rose researched investigational drugs to be prepared in the event of a relapse. Her husband died February 12, 2021 with a rare and unexplained occurrence of liver cancer possibly unrelated to AML.

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