Célia A. Aveleira
+ 351 918731966
celia.aveleira@uc.pt
Invited Scientist
Group at CNC
Education: 

I got my BSc degree in Biology in 2002 at the University of Coimbra (UC), Portugal. I then received a FCT Research Fellowship to work at IBILI-Faculty of Medicine, UC, under the project “Mechanisms of cell degeneration in diabetic retinopathy”. In 2005, I began my PhD studies as a FCT-grantee at IBILI, focusing on the role of inflammatory cytokines on blood-retinal barrier dysfunction in diabetic retinopathy. After spending 2 years at Penn State University College of Medicine (USA), to acquire advanced training and complement my PhD research, I concluded my PhD in Biomedical Sciences in 2010, at the Faculty of Medicine, UC.
After that, I became a postdoctoral researcher (FCT grantee) at the Center for Neuroscience and Cell Biology (CNC), UC, and began to study the potential role of neuropeptide Y (NPY) as a mimetic of caloric restriction, the most robust anti-aging strategy. In 2013 I was appointed as Invited Scientist at CNC (my current position) under the project “Aging, Stress and Chronic Diseases: From Mechanisms to Therapeutics”. With a focus on the role of caloric restriction mimetics as therapeutics targets to delay the aging process, I recently extended my research scope to tackle premature aging diseases, particularly Progeria.
I am author/co-author of 15 papers in international peer-reviewed journals, 10 of them published in Q1 journals. I am the PI of 1 research project (Progeria Research Foundation, USA) and was team member in 7 previously funded ones. Along with scientific research, I also actively contribute to students’ training: 2 MSc students as principal supervisor; 2 PhD, 1 MSc and 7 BSc’s students as co-supervisor. Moreover, I participated in several MSc and PhD programs from UC with invited lectures, and as member in academic examining committees of MSc thesis.

Afiliation: 

CNC

Area of Research: 

The increase in human life expectancy and the socioeconomic burden of age-related diseases has created a demand for effective interventions to delay aging. My main research goal is thus to find novel therapeutic strategies to delay aging. To this end, I am investigating the role of caloric restriction mimetics as therapeutics targets to delay the aging process of normal and premature aging diseases, such as Hutchinson-Gilford progeria syndrome (HGPS). My scientific interests cross three interconnected areas: 1) Aging; 2) Neuroendocrinology (Hypothalamic control of Aging); and 3) Metabolism.

 

Research Summary: 
http://orcid.org/0000-0002-2191-0682
Selected Publications: 

Aveleira CA*, Botelho M*, Carmo-Silva S, Pascoal JF, Ferreira-Marques M, Nóbrega C, Cortes L, Valero J, Sousa-Ferreira L, Álvaro AR, Santana M, Kügler S, Pereira de Almeida L, Cavadas C. Neuropeptide Y stimulates autophagy in hypothalamic neurons. PNAS 2015, 112(13):E1642-51. IF: 9.809; Q1 *equal contribution

Aveleira CA*, Botelho M*, Cavadas C. Neuropeptide Y stimulates autophagy in hypothalamic neurons: a caloric restriction mimetic. Autophagy 2015, 11(8):1431-3. IF: 11.423; Q1 *equal contribution

Sousa-Ferreira L, Álvaro AR, Aveleira C, Santana M, Brandão I, Kügler S, de Almeida LP, Cavadas C. Proliferative hypothalamic neurospheres express NPY, AGRP, POMC, CART and Orexin-A and differentiate to functional neurons. PLoS One 2011, 6(5):e19745. IF: 3.534; Q1

Sousa-Ferreira L, Aveleira C, Botelho M, Alvaro AR, Pereira de Almeida L, Cavadas C. Fluoxetine induces proliferation and inhibits differentiation of hypothalamic neuroprogenitor cells in vitro. PLoS One 2014, 9(3):e88917. IF: 3.534; Q1

Aveleira CA, Lin CM, Abcouwer SF, Ambrósio AF, Antonetti DA. TNF-α signals through protein kinase C zeta (PKCζ)/nuclear factor-kappa B (NF-κB) to alter the tight junction complex and increase retinal endothelial cell permeability. Diabetes 2010, 59(11):2872-82. IF: 8.474; Q1ypothalamic neurons. PNAS 2015, 112(13):E1642-51. IF: 9.809; Q1 *equal contribution

Other information: 

http://neuroendocrinologyandaging-cnc.weebly.com/phd.html

 
   
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