Age-related decline in circulating IGF-1 associates with impaired neurovascular coupling responses in older adultsShow others and affiliations
2022 (English)In: GeroScience, ISSN 2509-2715, Vol. 44, no 6, p. 2771-2783Article in journal (Refereed) Published
Abstract [en]
Impairment of moment-to-moment adjustment of cerebral blood flow (CBF) to the increased oxygen and energy requirements of active brain regions via neurovascular coupling (NVC) contributes to the genesis of age-related cognitive impairment. Aging is associated with marked deficiency in the vasoprotective hormone insulin-like growth factor-1 (IGF-1). Preclinical studies on animal models of aging suggest that circulating IGF-1 deficiency is causally linked to impairment of NVC responses. The present study was designed to test the hypotheses that decreases in circulating IGF-1 levels in older adults also predict the magnitude of age-related decline of NVC responses. In a single-center cross-sectional study, we enrolled healthy young (n = 31, 11 female, 20 male, mean age: 28.4 + / - 4.2 years) and aged volunteers (n = 32, 18 female, 14 male, mean age: 67.9 + / - 4.1 years). Serum IGF-1 level, basal CBF (phase contrast magnetic resonance imaging (MRI)), and NVC responses during the trail making task (with transcranial Doppler sonography) were assessed. We found that circulating IGF-1 levels were significantly decreased with age and associated with decreased basal CBF. Age-related decline in IGF-1 levels predicted the magnitude of age-related decline in NVC responses. In conclusion, our study provides additional evidence in support of the concept that age-related circulating IGF-1 deficiency contributes to neurovascular aging, impairing CBF and functional hyperemia in older adults.
Place, publisher, year, edition, pages
Springer, 2022. Vol. 44, no 6, p. 2771-2783
Keywords [en]
Aging, cognitive decline, neurovascular uncoupling, VCI, VCID, vascular cognitive impairment
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-113747DOI: 10.1007/s11357-022-00623-2ISI: 000829985600001PubMedID: 35869380Scopus ID: 2-s2.0-85134469806OAI: oai:DiVA.org:oru-113747DiVA, id: diva2:1859513
Note
Funding Agency:
University of Pecs
2024-05-222024-05-222024-05-22Bibliographically approved