Targeting the mitochondria-tyr kinase axis to prevent age-associated neuronal decline

JPI HDHL JFA “Nutrition and Cognitive Function” (NutriCog)
Targeting the mitochondria-tyr kinase axis to prevent age-associated neuronal decline
Natascia Ventura
Institute of Clinical Chemistry and Laboratory Medicine
Partner Organization Partner Country
IUF – Leibniz Research Institute for Environmental MedicineGermany
University of RomeItaly
Centro de Biologia MolecularSpain

1. Overall project description

1.1 Summary

Please summarise the main objectives and the overall achievements of the consortium and the
expected impact of the project results Mitochondria represent central regulators of nutritional homeostasis and of the aging process.Epidemiological studies, including data from our cohort, indicate nutritional risk and preventive factors associated with dietary intake for the development of age-related parameters. Notably, studies from
this network revealed the importance of a finely tuned mitochondria-autophagy axis as a preventive
mechanism against aging. However, whether and how specific dietary interventions can modulate
mitochondrial function in turn impacting on age-associated neuronal and cognitive decline is largely
unknown. Tyr-kinases are emerging as important regulators of mitochondrial function and have been
implicated in the development of age-associated disorders. In our consortia we want to specifically
address whether selected nutrients, mainly polyphenols founds in fruits and vegetables, regulate a
mitochondria-tyr kinase crosstalk, to delay/prevent the neuronal and cognitive decline observed during
physiological and accelerated aging.

Through four distinct but complementary working packages our specific aims are: (i) to assess
whether selected nutritional factors are associated with and can delay age-associated neuronal
changes (WP1-2); (ii) to unravel underlying molecular mechanisms of selected nutritional factors
through targeted (i.e. the mitochondrial-tyr kinases axis) and unbiased approaches (i.e. GWAS and –
omics studies (WP1-3); (iii) to assess the implications of relevant pathways and interventions to
alleviate cognitive disorders in mice (WP1&4).

This proposal brings together an original combination of complementary model systems and expertise
to untangle novel molecular mechanisms for selected nutritional factors in protecting against ageassociated
cognitive disorders. A key asset of our network is the coupling of basic experimental
research using different model systems (i.e. in vitro mechanistic studies on mammalian cells; in vivo
lifespan and neuronal behavioral assays in C. elegans and mice) and epidemiological research
(association studies on the SALIA longitudinal cohort for pre-dementia disorders). Through this
interdisciplinary, transnational work, the present consortium will therefore ultimately deliver biological
outputs that may suggest novel molecular mechanisms and preventive strategies for future clinical
studies. Specifically, this research initiative will provide a better understanding of the role of
mitochondria-tyr kinase crosstalk as a possible target denominator for preventive strategies against
the neuronal and cognitive decline observed during aging. In particular the assessment of selected
nutrients, mainly polyphenols founds in fruits and vegetables, as regulators of mitochondrial
functionality and thus possibly acting as preventive factors (together with susceptibility genes) to delay
age of onset, development and severity of age-related neurodegenerative processes and in particular
cognitive disorders. Our project is therefore expected to provide guidelines for clinicians to interpret
potential effects of nutritional factors thus contributing to the knowledge for the preventive potential of
diet on cognitive disorders.

1.2 Highlights

4. Impact

4.1 List of publications

AuthorsTitleYear, Issue, PPDoiPdf

4.2 Presentation of the project

Target groupAuthorsMeans of communicationHyperlinkPdf

4.3 List of submitted patents and other outputs

Patent licencePartners involvedYearInternational eu or national patentCommentPdf


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