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Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry

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Human Monocytes Plasticity in Neurodegeneration.

Ilenia Savinetti¹, Angela Papagna¹, Maria Foti¹

¹School of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.

|July 2, 2021

Summary

Monocytes, key immune cells, are implicated in neurodegenerative diseases like Alzheimer's and Parkinson's. Understanding monocyte dysregulation in the brain and body is crucial for developing new treatments.

Keywords:

epigenetics gene expression human monocytes innate immunity neurodegeneration single cells analysis trained immunity

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Area of Science:

Immunology
Neuroscience
Pathology

Background:

Monocytes are critical immune cells involved in inflammation and tissue repair.
Their heterogeneity suggests diverse functions and potential roles in disease.
Emerging evidence links monocyte infiltration into the brain with neurodegenerative conditions.

Purpose of the Study:

To review the current understanding of monocyte dysregulation in neurological diseases.
To explore the correlation between peripheral and central monocyte activity and neurodegeneration.

Main Methods:

Literature review of studies investigating monocyte function in neurodegenerative diseases.
Analysis of research on monocyte infiltration and activation in the central nervous system.
Synthesis of data on monocyte involvement in Alzheimer's, Parkinson's, ALS, and MS.

Main Results:

Monocyte dysregulation is increasingly recognized as a factor in neurodegenerative disease pathogenesis.
Evidence supports a role for monocytes in both initiating and exacerbating neurological damage.
Specific monocyte subsets may have distinct impacts on disease progression.

Conclusions:

Monocytes represent a significant therapeutic target for neurodegenerative disorders.
Further research into monocyte biology is essential for novel treatment strategies.
Targeting monocyte pathways could offer new avenues for managing Alzheimer's, Parkinson's, ALS, and MS.