In a recent study published in the Proceedings of the National Academy of Sciences Journal, researchers examined the therapeutic effects of targeting integrins for treating Amyotrophic lateral sclerosis (ALS) disease.
Study: Elevated α5 integrin expression on myeloid cells in motor areas in amyotrophic lateral sclerosis is a therapeutic target. Image Credit: DavidHerraezCalzada/Shutterstock.com
Background
ALS is a neurodegenerative disease that causes the motor cortex, brainstem, and spinal cord to lose motor neurons over time, leading to paralysis and death. In the United States, three approved treatments slow down the progression of ALS.
It is characterized by motor neuron degeneration. However, several studies show that immune cells from the blood and glial cells from the central nervous system (CNS) and peripheral nervous system (PNS) influence neurodegeneration in familial and sporadic ALS, challenging the neuron-centric theory.
There has been discussion about whether inflammation is a cause or result of ALS. A systems immunology analysis using mass cytometry (CyTOF) predicted the proinflammation role of α-integrins in late-stage of superoxide dismutase-1 G93A (SOD1G93A) mice microglia and peripheral nerve macrophages.
In the present study, researchers explored the potential of targeting α5 integrin as a therapeutic approach to modulate neuroinflammation in ALS.
About the study
This study used hSOD1G93A transgenic mouse lines for histopathology experiments. The mice carrying the human SOD1 transgene were identified through polymerase chain reaction (PCR) screening of tail deoxyribonucleic acid (DNA).