Abstract Description
Plenary Debate
Painful diabetic neuropathy (PDN) represents a significant challenge in clinical management, necessitating a comprehensive understanding of its underlying pathophysiology to develop effective interventions. As the research community strives to bridge the gap between preclinical models and clinical reality, this plenary debate aims to critically examine the translational potential of mouse models in the context of PDN.
Pall Karlsson will delve into the intricacies of this debate, unraveling the complexities that surround the utilization of mouse models to study PDN. The talk will shed light on the limitations of these models, prompting a reflection on the broader implications for clinical translation.
The differences in pain or nociception often observed in animal models versus human patients, serves as a one of the key focal points. Karlsson will navigate through the implications of this distinction, addressing whether these models truly capture the essence of human PDN. Are we, and can we, measure pain in animals? By critically assessing the behavioral endpoints employed in mouse and rodent studies, the presentation aims to offer a nuanced perspective on the relevance of these models to human chronic pain experiences.
Another salient theme explored in the talk is the structural and functional discrepancies that emerge between rodents and humans. Karlsson will dissect the fundamental differences in neuropathy pathogenesis. This analysis forms the basis for an argument that challenges the predictive value of rodent models for therapeutic efficacy in human PDN.
Novel behavioral tests that mirror human experiences are emerging, although their utility and validity warrant critical examination. The inclusion of these evolving techniques in the discourse offers a glimpse into the future possibilities for bridging the gap. Lastly, Karlsson will spotlight the historical context of translational successes and setbacks.
Learning Objectives
1. Analyze the key distinctions of pain sensations in rodent models for painful diabetic neuropathy (PDN), discerning their implications for translational relevance in the context of human chronic pain experiences.
2. Evaluate the structural and functional discrepancies between rodent and human neuropathy, assessing their influence on the predictability of rodent models for therapeutic efficacy in the treatment of painful diabetic neuropathy (PDN).
3. Critique the role of rodent models as a translational bridge for painful diabetic neuropathy (PDN) research, formulating strategies to align preclinical investigations with clinical trial priorities, enhancing the likelihood of attracting funding and expediting therapeutic advancements.
Moderator: Dr. David Bennett
Painful diabetic neuropathy (PDN) represents a significant challenge in clinical management, necessitating a comprehensive understanding of its underlying pathophysiology to develop effective interventions. As the research community strives to bridge the gap between preclinical models and clinical reality, this plenary debate aims to critically examine the translational potential of mouse models in the context of PDN.
Pall Karlsson will delve into the intricacies of this debate, unraveling the complexities that surround the utilization of mouse models to study PDN. The talk will shed light on the limitations of these models, prompting a reflection on the broader implications for clinical translation.
The differences in pain or nociception often observed in animal models versus human patients, serves as a one of the key focal points. Karlsson will navigate through the implications of this distinction, addressing whether these models truly capture the essence of human PDN. Are we, and can we, measure pain in animals? By critically assessing the behavioral endpoints employed in mouse and rodent studies, the presentation aims to offer a nuanced perspective on the relevance of these models to human chronic pain experiences.
Another salient theme explored in the talk is the structural and functional discrepancies that emerge between rodents and humans. Karlsson will dissect the fundamental differences in neuropathy pathogenesis. This analysis forms the basis for an argument that challenges the predictive value of rodent models for therapeutic efficacy in human PDN.
Novel behavioral tests that mirror human experiences are emerging, although their utility and validity warrant critical examination. The inclusion of these evolving techniques in the discourse offers a glimpse into the future possibilities for bridging the gap. Lastly, Karlsson will spotlight the historical context of translational successes and setbacks.
Learning Objectives
1. Analyze the key distinctions of pain sensations in rodent models for painful diabetic neuropathy (PDN), discerning their implications for translational relevance in the context of human chronic pain experiences.
2. Evaluate the structural and functional discrepancies between rodent and human neuropathy, assessing their influence on the predictability of rodent models for therapeutic efficacy in the treatment of painful diabetic neuropathy (PDN).
3. Critique the role of rodent models as a translational bridge for painful diabetic neuropathy (PDN) research, formulating strategies to align preclinical investigations with clinical trial priorities, enhancing the likelihood of attracting funding and expediting therapeutic advancements.
Moderator: Dr. David Bennett
