Overlapping Neuroimmune Mechanisms and Therapeutic Targets in Neurodegenerative Disorders

Many potential immune therapeutic targets are similarly affected in adult-onset neurodegenerative diseases, such as Alzheimer's (AD) disease, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD), as well as in a seemingly distinct Niemann-Pick type C disease with primarily juvenile onset. This strongly argues for an overlap in pathogenic mechanisms. The commonly researched immune targets include various immune cell subsets, such as microglia, peripheral macrophages, and regulatory T cells (Tregs); the complement system; and other soluble factors. In this review, we compare these neurodegenerative diseases from a clinical point of view and highlight common pathways and mechanisms of protein aggregation, neurodegeneration, and/or neuroinflammation that could potentially lead to shared treatment strategies for overlapping immune dysfunctions in these diseases. These approaches include but are not limited to immunisation, complement cascade blockade, microbiome regulation, inhibition of signal transduction, Treg boosting, and stem cell transplantation.

Automated summary

There is an overlap in immune therapeutic targets between adult-onset neurodegenerative diseases and juvenile-onset Niemann-Pick type C disease, suggesting common pathogenic mechanisms. The review compares these diseases from a clinical perspective and highlights shared pathways and mechanisms of protein aggregation, neurodegeneration, and/or neuroinflammation. This could potentially lead to shared treatment strategies for immune dysfunctions in these diseases.