Neurodegeneration and Neuroinflammation in Parkinson's Disease: a Self-Sustained Loop.
Giuseppe ArenaK SharmaG AgyeahR KrügerA GrünewaldJ C FitzgeraldPublished in: Current neurology and neuroscience reports (2022)
Cell autonomous alterations in neuronal cells, including mitochondrial damage and protein aggregation, could play a role, but recent findings also highlighted the importance of intercellular communication at both local and systemic level. This has given rise to debate about the role of non-neuronal cells in PD and reignited intense research into the gut-brain axis and other non-neuronal interactions in the development of the disease. Whatever the original trigger of neuroinflammation in PD, what appears quite clear is that the aberrant activation of glial cells and other components of the immune system creates a vicious circle in which neurodegeneration and neuroinflammation nourish each other. In this review, we will provide an up-to-date summary of the main cellular alterations underlying neuroinflammation in PD, including those induced by environmental factors (e.g. the gut microbiome) and those related to the genetic background of affected patients. Starting from the lesson provided by familial forms of PD, we will discuss pathophysiological mechanisms linked to inflammation that could also play a role in idiopathic forms. Finally, we will comment on the potential clinical translatability of immunobiomarkers identified in PD patient cohorts and provide an update on current therapeutic strategies aimed at overcoming or preventing inflammation in PD.
Keyphrases
- induced apoptosis
- cerebral ischemia
- oxidative stress
- cell cycle arrest
- traumatic brain injury
- lipopolysaccharide induced
- lps induced
- cognitive impairment
- end stage renal disease
- endoplasmic reticulum stress
- stem cells
- newly diagnosed
- inflammatory response
- blood brain barrier
- ejection fraction
- chronic kidney disease
- transcription factor
- spinal cord injury
- early onset
- multiple sclerosis
- cell proliferation
- prognostic factors
- climate change
- white matter
- risk assessment
- neuropathic pain
- spinal cord
- patient reported outcomes