Angel Cedazo Minguez

Angel Cedazo Minguez

Professor
Telephone: +46852483527
Visiting address: Blickagången 6, 14157 Huddinge
Postal address: H1 Neurobiologi, vårdvetenskap och samhälle, H1 Neurogeriatrik Maioli, 171 77 Stockholm
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About me

  • My research is focused on understanding the molecular mechanism behind risk factor for neurodegenerative disorders. I combine my activities at KI with being Vice-president for Strategic Initiatives and Scientific Relations at Sanofi and I am located in Paris (France). So far, I have published 100+ articles and directed 10 PhD thesis. 

    Positions
    From 2017- Professor in Molecular Neurogeriatrics, KI
    From 2022- Vice-president. Strategic Initiatives and Scientific Relations. SANOFI
    From 2017- 2022 Head of Neurodegeneration Research, SANOFI
    From 2006- 2017 Deputy Head of KI-Alzheimer disease research center / Neurogeriatrics
    From 2014- 2017 Codirector of Swedish Brain Power. A national network of centers of excellence in Neurodegenerative disorders.
    From 2014- 2017 Vice-Head of the department of neurobiology, care sciences and society

    Education
    2017 Professor. Karolinska Institutet
    2011 Senior University Lecturer. Karolinska Institutet.
    2010 Associate Professor. Karolinska Institutet.
    2010 Course for future academic leaders (MAL). Karolinska Institutet.
    2002 Ph.D. in medicine (Neuroscience). Karolinska Institutet. Thesis: Apolipoprotein E and Alzheimer's disease: Signals and effects

    Academic honours, awards and prizes
    2013. Deputy Head (prefekt) of the Department of Neurobiology, Care Sciences and Society (NVS) at KI.
    2009-2012. Vice-Head of the Department of Neurobiology, Care Sciences and Society at KI
    2009- present. Member of the Committee for Research and Education at the Geriatric Department of the Swedish Medical Research Council (FoU råd)
    2006, 2007 and 2008. Erik Rönnbergs award for research in geriatric medicine from the Bank of Sweden Tercentenary Foundation
    2003 and 2004. Hjärnfonden postdoc (Swedish Brain Foundation)
    2003. Svenska Lundbeck stiftelsen.

Research

  • Over the years, genetic and epidemiological studies have reported gene or environmental factors that increase the risk for Alzheimer's Disease (AD), suggesting that it is a disease of multifactorial origin. We aim to contribute to understand the effects of risk factors for AD, and to define to which extent these factors are secondary actors or driving forces for cognitive decline.

    Apolipoprotein E, hypercholesterolemia and AD

    ApoE is the main cholesterol transporter and the presence of the E4 isoform is the major risk factor for AD. High cholesterol levels in blood is another risk factor. Our hypothesis is that ApoE4 acts in synergy with environmental factors (like hypercholesterolemia) to affect signaling pathways involved in neurodegeneration. We use several in vivo and in vitro models to explore this hypothesis.

    Functions of oxysterols in brain

    The metabolism of cholesterol results in the production of several oxysterols, of which the peripherally-produced 27OHC and the brain-produced 24S-OH have been suggested to play a role in AD pathogenesis. However very little is known about the biological role of these oxysterols, with the exception of its affinity for LXR receptors. We have discovered new functions of 24S-OH and 27OHC in brain, related with memory consolidation and vascular regulation. Our findings suggest that these molecules are much more than subproducts of the cellular metabolism, and can be regarded as signalling molecules of importance for normal brain function as well as for neurodegeneration.

    Thioredoxin and AD

    Oxidative stress (OS) is one of the pathological events occurring in AD. Thioredoxin-1 (TRX1) modulate the redox homeostasis and inhibit the apoptosis signal-regulating kinase (ASK1). We reported that the TRX1 levels is impaired in AD. We showed that Abeta neurotoxicity is mediated by TRX1 oxidations and ASK1 activation. Recently, we have described the presence of a truncated form of TRX1 (TRX80) in the brain. TRX80 is dramatically reduced in AD. Also we found that TRX80 as a protective role on Amyloid-beta neurotoxicity and aggregation. So, far TRX80 is the only endogenous anti-Amyloid beta aggregant peptide described.

Selected publications

Articles

All other publications

Employments

  • Professor, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, 2017-

Degrees and Education

  • Docent, Karolinska Institutet, 2010
  • Doctor Of Philosophy, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, 2002

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