Age-Related Midbrain Inflammation and Senescence in Parkinson’s Disease

Frontiers in Aging Neuroscience

Markus Riessland¹  Taylor Russo¹ 

[1] Center for Nervous System Disorders, Stony Brook University, Stony Brook, NY, United States;Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, United States;

关键词: Parkinson’s disease;    cellular senescence;    dopamine neurons;    immune response;    neuroinflammation;    aging;   

DOI  :  10.3389/fnagi.2022.917797

来源: DOAJ

【 摘 要 】

Immune responses are arising as a common feature of several neurodegenerative diseases, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Amyotrophic Lateral Sclerosis (ALS), but their role as either causative or consequential remains debated. It is evident that there is local inflammation in the midbrain in PD patients even before symptom onset, but the underlying mechanisms remain elusive. In this mini-review, we discuss this midbrain inflammation in the context of PD and argue that cellular senescence may be the cause for this immune response. We postulate that to unravel the relationship between inflammation and senescence in PD, it is crucial to first understand the potential causative roles of various cell types of the midbrain and determine how the possible paracrine spreading of senescence between them may lead to observed local immune responses. We hypothesize that secretion of pro-inflammatory factors by senescent cells in the midbrain triggers neuroinflammation resulting in immune cell-mediated killing of midbrain dopaminergic (DA) neurons in PD.

【 授权许可】

Unknown