Imagine you’re trying to solve a puzzle, but all the pieces you have are brand new and shiny. You might think you’re on the right track, but what if there’s a piece missing that only a weathered one can provide? That’s what scientists studying Parkinson’s disease (PD) have been doing for years – using young animal models to understand the disease. However, recent research suggests that overlooking the impact of aging could be holding them back from finding effective treatments. Just like weathering gives a puzzle piece character and clues, aging animals reveal important insights into the cellular and molecular mechanisms of PD. These older models not only develop PD pathology more easily, but also experience a faster and more widespread progression of the disease. By including aged animals in their studies, scientists can better mimic the clinical features of PD in humans, leading to more accurate results and increased potential for successful therapy development. If you’re curious to learn more about how researchers are addressing the challenges of using aged animal models, check out the full article!

Aging is the biggest risk factor for developing Parkinson’s disease (PD), the second most common neurodegenerative disorder. Several animal models have been developed to explore the pathophysiology underlying neurodegeneration and the initiation and spread of alpha-synuclein-related PD pathology, and to investigate biomarkers and therapeutic strategies. However, bench-to-bedside translation of preclinical findings remains suboptimal and successful disease-modifying treatments remain to be discovered. Despite aging being the main risk factor for developing idiopathic PD, most studies employ young animals in their experimental set-up, hereby ignoring age-related cellular and molecular mechanisms at play. Consequently, studies in young animals may not be an accurate reflection of human PD, limiting translational outcomes. Recently, it has been shown that aged animals in PD research demonstrate a higher susceptibility to developing pathology and neurodegeneration, and present with a more disseminated and accelerated disease course, compared to young animals. Here we review recent advances in the investigation of the role of aging in preclinical PD research, including challenges related to aged animal models that are limiting widespread use. Overall, current findings indicate that the use of aged animals may be required to account for age-related interactions in PD pathophysiology. Thus, although the use of older animals has disadvantages, a model that better represents clinical disease within the elderly would be more beneficial in the long run, as it will increase translational value and minimize the risk of therapies failing during clinical studies. Furthermore, we provide recommendations to manage the challenges related to aged animal models.

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