Ivan Nalvarte

Ivan Nalvarte

Senior Forskare | Docent
E-postadress: ivan.nalvarte@ki.se
Besöksadress: BioClinicum J9:20, Visionsgatan 4, 17165 Solna
Postadress: H1 Neurobiologi, vårdvetenskap och samhälle, H1 Neurogeriatrik Nalvarte, 171 77 Stockholm
Del av:

Om mig

  • Docent, Senior forskare. 

    Jag är gruppledare vid avdelningen för Neurogeriatrik vid institutionen för Neurobiologi, Vårdvetenskap och Samhälle (NVS).

    Lab-webbsida - Under uppbyggnad!

Forskningsbeskrivning

  • Min bakgrund är inom neuroendokrinologi och min forskning fokuserar på effekterna av könshormonsignalering på hjärnans åldrande. Ett huvudämne i min forskning är hur avvikande könshormonsignalering under endokrint känsliga livsstadier kan modulera risken för depressiva och neurodegenerativa tillstånd. För att uppnå detta är jag en del av ett nätverk av specialister som använder tvärvetenskapliga metoder, kombinerar epidemiologiska data med innovativ experimentell modellering och integrerar storskalig data för att driva detta forskningsområde framåt.

Undervisning

  • 2019-2023: Kursledare: Biomedicine Master program thesis work and
    examination, Karolinska Institutet
    2018- : Target Organ Toxicology, Nuclear receptor signalling and EDCs,  Karolinska Institutet
    2016- : Tutor in “Sex hormones and ESC differentiation”, Post-graduate
    course in Human Embryonic Stem Cells, 2212, Karolinska Institutet
    2015-: Responsible for the practicum in course Functional Genomics,
    Biomedicine Bachelor programme, Karolinska Institute, Stockholm, Sweden
    2014-2017: Applied Science Communication (ACB2), Biomedicine Master
    programme, Karolinska Institute, Stockholm, Sweden
    2013- : Applied Science Communication (ACB4), Biomedicine Master programme,
    Karolinska Institute, Stockholm, Sweden
    2014- : Tutor in “Proteomic techniques and applications”, Biomedicine
    Bachelor programme, Karolinska Institute, Stockholm, Sweden
    03/2012: Tutor in WiMo 2012 Wissenschaftsmonat für Medizinstudierende,
    theory, University of Basel, basel, Switzerland
    09-10/2011: Tutor in Introduction to Biology, theory. University of Basel,
    Basel, Switzerland
    2008-2009: Tutor in “Proteomic techniques and applications”, Molecular
    Nutrition undergraduate programme, Stockholm University, Stockholm, Sweden
    2008-2009: Responsible for the Theoretical and practical teaching in
    proteomics for researchers. Department of Biosciences and Nutrition,
    Karolinska Institute, Huddinge, Sweden
    2007-2009: Molecular biology. Theory and practice. Co-responsible for the
    course. Biomedicine undergraduate programme, Karolinska Institute, Stockholm,
    Sweden
    2002-2006: Teaching assistance at undergraduate courses in Molecular
    immunology, Molecular Biology, Cell Biology, and General Chemistry at
    Södertörns högskola and Karolinska Institute, Stockholm, Sweden.

Artiklar

Alla övriga publikationer

Forskningsbidrag

  • Swedish Research Council
    1 December 2024 - 30 November 2027
    Experimental research on Alzheimer´s disease (AD) relies heavily on mouse models, but these models poorly mimic human AD, leading to over 99% AD drugs failures in human trials. Consequently, there is an urgent need for more human-relevant experimental models of AD. However, the use of alternative human cell models is constrained due to the complex 3D multi-cellular nature of AD pathology, including an inflammatory component. In addition, their superiority over animal models remains uncertain, combined with insufficient validation regarding their relevance to human disease. To overcome this, we propose to benchmark a human forebrain organoid model of AD carrying amyloidogenic APPNL-G-Fmutations in co-culture with isogenic microglia immune cells. These organoids produce neurotoxic amyloid beta (Aβ), a hallmark of AD, and unlike AppNL-G-F mice they also produce hyperphosphorylated Tau protein, a second hallmark of AD. We will use a transcriptomic approach to ask: 1) are these organoids in any way superior to correspondingAppNL-G-F mice? 2): how well do they overlap with human AD pathology? And 3) are they functional in response to the amyloid-lowering drug Aducanumab? Answering these questions would give the first benchmarked and disease-validated AD organoid model and will be an important step towards promoting organoids’ wider use in AD research, thereby reducing the heavy reliance on mice while enhancing human relevance.
  • Swedish Research Council
    1 January 2024 - 31 December 2026
    APOE variant 4 is the most common genetic risk factor for late-onset Alzheimer’s disease (AD), and it is well known that women carrying APOE4 run a 4-fold higher risk of AD than male carriers. Nevertheless, the cause of this sex difference is still enigmatic. In this project, we address the hypothesis that the drop of female sex hormone estrogen and metabolic changes at menopause impact on APOE4 regulation and downstream factors, and that this contributes to sex differences in AD. Our preliminary results support this hypothesis by suggesting that the estrogen receptor beta (ERβ) to be an important link between menopause and APOE levels. Selective ERβ activation protects against AD pathology in an AD mouse model and can regulate APOE levels in a sex-specific manner. Making use of a multidisciplinary collaboration between experts in neuroendocrinology, AD, epidemiology, biostatistics, and genetics, we will:address the relationship between age at menopause, hormone replacement therapy, APOE4 and other genetic variants, and AD diagnosis in human cohorts,validate such relationships in an AD mouse model where menopause is simulated, andin a data-driven approach identify causative molecular networks underlying these relationships using human APOE4 brain organoid models.The outcome of this project will provide new mechanistic insights into the sex differences in AD and how such knowledge can be used for preventive clinical measures, especially for APOE4-positive women.
  • Using epigenomics to identify Alzheimer’s disease risk in gender dysphoria
    Alzheimer's Association
    1 January 2024 - 31 December 2026
  • A new model to study Alzheimer’s disease in human mini-brains
    Forska Utan Djurförsök
    1 January 2024 - 31 December 2025
  • European Commission
    1 January 2023 - 31 December 2027
  • Ultra-sensitive multiplex detection of inflammatory and pathological markers in diseases such as Alzheimer’s disease, kidney disease and Covid19
    Ingabritt och Arne Lundbergs forskningstiftelse
    1 January 2023 - 31 December 2024
  • Estrogen receptor beta in Alzheimer’s disease
    KID Funding
    1 March 2022 - 28 February 2026
  • Karolinska Institutet Stiftelser
    Karolinska Institutet Stiftelser
    1 January 2021 - 31 December 2024
  • National Institute on Aging
    30 September 2020 - 31 May 2024
  • Organoids as preclinical model of Parkinson
    STINT
    1 July 2019 - 30 June 2022
  • Swedish Research Council
    1 January 2018 - 31 December 2021

Anställningar

  • Senior Forskare, Neurobiologi, vårdvetenskap och samhälle, Karolinska Institutet, 2024-

Examina och utbildning

  • Docent, Molekylär endokrinologi, Karolinska Institutet, 2018
  • MEDICINE DOKTORSEXAMEN, Institutionen för biovetenskaper och näringslära, Karolinska Institutet, 2006
  • Medicine Kandidatexamen, Karolinska Institutet, 1998

Gästforskning och resestipendier

  • Postdoc, Friedrich Miescher Institute, Postdoc, 2010-2013

Nyheter från KI

Kalenderhändelser från KI