FLI Seminar with Cláudia Cavadas

In this seminar, I will present my previous and recent research on strategies to delay aging and age-related diseases, inspired by hypothalamic functions and brain–periphery communication.

I will show that caloric restriction induces autophagy in hypothalamic and cortical neurons, mediated in part by NPY and ghrelin receptors activation. I will also show that NPY itself stimulates hypothalamic autophagy, and that restoring NPY levels in a premature aging mouse model rescued aging markers, including memory deficits. Moreover, I will present evidence that ghrelin treatment improved molecular and histopathological features of aging and extended lifespan in a Progeria mouse model.

I will also present my work on Machado-Joseph disease (MJD). In mouse models, caloric restriction, Sirtuin 1 overexpression, or NPY mitigated motor and balance impairments and cerebellar pathology. In addition, I found circadian rhythm disruption in patients and preclinical models, opening new therapeutic targets.

Finally, I will discuss a novel hypothesis: peripheral senescence can remotely influence brain aging. Transplanting senescent skin fibroblasts into young mice induced frailty, impaired musculoskeletal and cognitive functions, and increased hippocampal senescence markers. These findings support that senescent cells in the skin can drive systemic aging and brain decline.

My research underscores the pivotal role of neuroendocrine mechanisms—particularly hypothalamic function and brain–periphery communication—in regulating aging and age-related diseases.

Cláudia Cavadas is PharmD and PhD in Pharmacology, University of Coimbra, Portugal. She is the head of the Neuroendocrinology and Aging Group at CNC - Center for Neuroscience and Cell Biology. Her research group has the mission is to contribute to develop new knowledge in the aging field and age-related disorders. 

For more information

Cláudia Cavadas, University of Coimbra, Portugal

The seminar will be held as an in-person event.