Although numerous independent studies have provided evidence for the involvement of central and peripheral inflammatory and immune processes in Parkinson’s disease, determining a causal relationship between neuroinflammation and neurodegeneration has not yet been established. The menstrual cycle in Parkinson’s disease is difficult to determine because the initiating event(s) occurred many years earlier. neuronal loss and clinical manifestations arise. However, there is growing evidence that inflammation may play a role in Parkinson’s disease rather than as a consequence or side effect of the neurodegenerative process.
“The risk of PD is influenced by many factors, including a combination of immunological and environmental genetics, such as history of infection,” comments Bastiaan R. Bloem, MD, PhD; Patrik Brundin, MD, PhD; Dr. Ashley Harms; Cecilia Lindestam Arlehamn, PhD, Eng King Tan, MD; and Dr. Caroline Williams-Grey. Various experimental models developed in recent years show evidence of an association between an autoimmune condition and the immune system or its abnormal response in patients with Parkinson’s disease.
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Topics include different test models:
- Immunological determinants of PD
- Epidemiological evidence for an immune component of PD
- Effects of infection and microbiome
- Link between GBA1 gene and immunological changes in PD
- The role of T lymphocytes
- The role of B . lymphocytes
- Natural killer cells in PD
- Age-related immune changes in PD
- Microscopic activation in the brains of patients with neurodegenerative disorders including PD
- Current evidence and knowledge gaps surrounding inflammasome activation in PD
- The role of central and peripheral inflammation
- Neuritis and immune changes in PD . prodromal
- Inflammatory animal model of PD
- Biomarkers of inflammation in PD
- Therapeutic strategies targeting the immune system in PD
A review by Benjamin D. Hobson, MD/PhD fellow, and David Sulzer, PhD, both of Columbia University Irving Medical Center, focuses on how peripheral T lymphocytes are can invade the brain regions primarily affected in Parkinson’s disease.
Recent research on Parkinson’s disease
Neurons in these brain regions can present antigens that bind to major histocompatibility complex (MHC) class 1 molecules on the cell surface and signal the physiological state of the cell for immune cells (such as T cells). Several subtypes of T cells (CD8+) have been shown to bind to antigen:MHC class 1 complexes on the cell surface, promoting subsequent immune responses leading to cell damage and ultimately is nerve cell death.
“Recent animal models show the ability of T cells to self-react to mitochondrial antigens in Parkinson’s disease,” Dr. Sulzer noted. “However, it remains unclear whether neuronal antigen presentation plays a role in Parkinson’s disease or other neurodegenerative disorders, and efforts are underway to better understand its effects. potential effects of autoimmune responses on neurodegenerative processes.”
In summary, numerous independent studies in clinical and preclinical models have provided corroborating evidence for the involvement of central and peripheral inflammatory and immune processes in Parkinson’s disease. Guest trainees note. “Our knowledge of how the immune system contributes to PD pathogenesis is constantly evolving, with growing evidence for the role of several susceptibility genes and loci.”
A major challenge is using these data and knowledge to identify specific targets in the immune system or to target key pathogenic proteins involved in abnormal immune responses; and potentially identify subsets of patients more likely to respond to immunomodulatory therapies.
“Clinical trials targeting alpha-synuclein have begun and both clinical trials and trials focusing on different immune components are ongoing,” guest co-editor and co-editor by JPD Bastiaan R. Bloem, MD, PhD, Center for Expertise in Parkinson’s & Movement Disorders, Radboud University Medical Center, Nijmegen.
The guest editors emphasize that considerable research is still needed to determine the individual and collective roles of individual immune cells (and their subsets) and how they interact with each other in neurovascular units and with alpha-synuclein and other important proteins.
“Longitudinal studies using molecular imaging to measure glial microglial activation in the brain, and detailed blood and cerebrospinal fluid immune function tests and phenotypes in at-risk subjects. myopathy or prodromal Parkinson’s disease may identify important clues about the temporal cause-and-effect relationship between neuroinflammation and Parkinson’s disease,” said Prof. Bloem concluded.
Parkinson’s disease is a slowly progressive disorder that affects movement, muscle control, and balance. It is the second most common age-related neurodegenerative disorder, affecting about 3% of the population over the age of 65 and up to 5% of people over the age of 85.
Source: Eurekalert
