In the complex world of Parkinson’s disease (PD), various factors like genes, environment, and age play a role in its development. Imagine PD as a puzzle with missing pieces. Researchers wanted to understand how these pieces fit together, so they zoomed in on mutant mice. These mice were treated with a low dose of rotenone, a chemical that mimics certain aspects of PD. By examining behavior and pathology, researchers discovered that older mice experienced more severe impairments in motor and olfactory functions compared to younger mice. They also noted increased loss of dopaminergic neurons in older mice with rotenone treatment. Furthermore, inflammation markers increased in the brains of older mice, along with changes in gut health. Interestingly, these effects were more pronounced as the mice aged. This research highlights how age interacts with genetic and environmental factors to deepen our understanding of PD. So grab your detective hat and dive deeper into this fascinating field of study by exploring the full article link below!

Multiple factors such as genes, environment, and age are involved in developing Parkinson’s disease (PD) pathology. However, how various factors interact to cause PD remains unclear. Here, 3-month and 9-month-old hα-syn+⁣/− mice were treated with low-dose rotenone for 2 months to explore the mechanisms that underline the environment–gene–age interaction in the occurrence of PD. We have examined the behavior of mice and the PD-like pathologies of the brain and gut. The present results showed that impairments of the motor function and olfactory function were more serious in old hα-syn+/– mice with rotenone than that in young mice. The dopaminergic neuron loss in the SNc is more in old hα-syn+/– mice with rotenone than in young mice. Expression of hα-syn+/– is increased in the SNc of hα-syn+/– mice following rotenone treatment for 2 months. Furthermore, the number of activated microglia cells increased in SNc and accompanied the high expression of inflammatory cytokines, namely, TNF-α and IL-18 in the midbrain of old hα-syn+/– mice treated with rotenone. Meanwhile, we found that after treatment with rotenone, hα-syn positive particles deposited in the intestinal wall, intestinal microflora, and T lymphocyte subtypes of Peyer’s patches changed, and intestinal mucosal permeability increased. Moreover, these phenomena were age-dependent. These findings suggested that rotenone aggravated the PD-like pathologies and affected the brain and gut of human α-syn+/– transgenic mice in an age-dependent manner.

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