Clinical Trials Targeting Aging

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Dokumenter

  • Fulltext

    Forlagets udgivne version, 912 KB, PDF-dokument

The risk of morbidity and mortality increases exponentially with age. Chronic inflammation, accumulation of DNA damage, dysfunctional mitochondria, and increased senescent cell load are factors contributing to this. Mechanistic investigations have revealed specific pathways and processes which, proposedly, cause age-related phenotypes such as frailty, reduced physical resilience, and multi-morbidity. Among promising treatments alleviating the consequences of aging are caloric restriction and pharmacologically targeting longevity pathways such as the mechanistic target of rapamycin (mTOR), sirtuins, and anti-apoptotic pathways in senescent cells. Regulation of these pathways and processes has revealed significant health- and lifespan extending results in animal models. Nevertheless, it remains unclear if similar results translate to humans. A requirement of translation are the development of age- and morbidity associated biomarkers as longitudinal trials are difficult and not feasible, practical, nor ethical when human life span is the endpoint. Current biomarkers and the results of anti-aging intervention studies in humans will be covered within this paper. The future of clinical trials targeting aging may be phase 2 and 3 studies with larger populations if safety and tolerability of investigated medication continues not to be a hurdle for further investigations.
OriginalsprogEngelsk
Artikelnummer820215
TidsskriftFrontiers in Aging
Vol/bind3
Antal sider10
ISSN2673-6217
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
This research was supported by the Novo Nordisk Foundation Challenge Programme (#NNF17OC0027812), the Nordea Foundation (#02-2017-1749), the Neye Foundation, the Lundbeck Foundation (#R324-2019-1492 and #R303-2018-3159), the Ministry of Higher Education and Science (#0238-00003B), VitaDAO and Insilico Medicine.

Publisher Copyright:
Copyright © 2022 Nielsen, Bakula and Scheibye-Knudsen.

Antal downloads er baseret på statistik fra Google Scholar og www.ku.dk


Ingen data tilgængelig

ID: 372181232