This study investigates the role of inflammation in the degeneration of dopamine (DA) neurons in an animal model of Parkinson's disease (PD). The researchers used a non-toxic dose of lipopolysaccharide (LPS) to induce inflammation in the substantia nigra (SN) of rats, followed by a low dose of 6-hydroxydopamine (6-OHDA) to simulate the early stages of PD. They found that preexisting inflammation increased the vulnerability of DA neurons to 6-OHDA-induced degeneration, with a significant increase in the number of TH-positive neurons lost in the SN. The inflammation was associated with increased levels of interleukin-1beta (IL-1β) and microglial activation. Administration of an interleukin-1 receptor antagonist significantly reduced the loss of TH-positive neurons, suggesting that IL-1β plays a crucial role in this process. These findings provide insights into the etiology of PD and highlight the potential of inflammation as a risk factor for neurodegenerative diseases.This study investigates the role of inflammation in the degeneration of dopamine (DA) neurons in an animal model of Parkinson's disease (PD). The researchers used a non-toxic dose of lipopolysaccharide (LPS) to induce inflammation in the substantia nigra (SN) of rats, followed by a low dose of 6-hydroxydopamine (6-OHDA) to simulate the early stages of PD. They found that preexisting inflammation increased the vulnerability of DA neurons to 6-OHDA-induced degeneration, with a significant increase in the number of TH-positive neurons lost in the SN. The inflammation was associated with increased levels of interleukin-1beta (IL-1β) and microglial activation. Administration of an interleukin-1 receptor antagonist significantly reduced the loss of TH-positive neurons, suggesting that IL-1β plays a crucial role in this process. These findings provide insights into the etiology of PD and highlight the potential of inflammation as a risk factor for neurodegenerative diseases.