The Effect of Mild Traumatic Brain Injury on Cerebral Microbleeds in AgingShow others and affiliations
2021 (English)In: Frontiers in Aging Neuroscience, E-ISSN 1663-4365, Vol. 13, article id 717391
Article in journal (Refereed) Published
Abstract [en]
A traumatic brain injury (TBI) induces the formation of cerebral microbleeds (CMBs), which are associated with cognitive impairments, psychiatric disorders, and gait dysfunctions in patients. Elderly people frequently suffer TBIs, especially mild brain trauma (mTBI). Interestingly, aging is also an independent risk factor for the development of CMBs. However, how TBI and aging may interact to promote the development of CMBs is not well established. In order to test the hypothesis that an mTBI exacerbates the development of CMBs in the elderly, we compared the number and cerebral distribution of CMBs and assessed them by analysing susceptibility weighted (SW) MRI in young (25 +/- 10 years old, n = 18) and elder (72 +/- 7 years old, n = 17) patients after an mTBI and in age-matched healthy subjects (young: 25 +/- 6 years old, n = 20; aged: 68 +/- 5 years old, n = 23). We found significantly more CMBs in elder patients after an mTBI compared with young patients; however, we did not observe a significant difference in the number of cerebral microhemorrhages between aged and aged patients with mTBI. The majority of CMBs were found supratentorially (lobar and basal ganglion). The lobar distribution of supratentorial CMBs showed that aging enhances the formation of parietal and occipital CMBs after mTBIs. This suggests that aging and mTBIs do not synergize in the induction of the development of CMBs, and that the different distribution of mTBI-induced CMBs in aged patients may lead to specific age-related clinical characteristics of mTBIs.
Place, publisher, year, edition, pages
Frontiers Media S.A., 2021. Vol. 13, article id 717391
Keywords [en]
Microhemorrhage, aging, cognitive decline, TBI, microvascular injury
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-113247DOI: 10.3389/fnagi.2021.717391ISI: 000708951000001PubMedID: 34658836Scopus ID: 2-s2.0-85117081169OAI: oai:DiVA.org:oru-113247DiVA, id: diva2:1853407
Funder
NIH (National Institutes of Health), R01-AG055395; R01-NS100782; R01-AT006526
Note
This work was supported by grants from the National Research, Development and Innovation Office to PT (NKFI-FK123798) and AB (K-134555), the Hungarian Academy of Sciences Bolyai Research Scholarship to PT, UNKP-20-3-II-PTE-493 New National Excellence Program of the Ministry for Innovation and Technology to PT and LT, EFOP-3.6.2.-16-2017-00008, GINOP-2.3.2-15-2016-00048, GINOP-2.2.1-15-2017-00067 to PT and AB, Hungarian Brain Research Program 2.0 Grant No. 2017-1.2.1-NKP-2017-00002 to AB, the Higher Education Institutional Excellence Programme of the Ministry of Human Capacities to PT and AB, Thematic Excellence Program 2020-4.1.1-TKP2020 National Excellence Sub-program to LT, the National Institute of Health R01-AG055395, R01-NS100782, R01-AT006526 to ZU. This study was funded by the Hungarian Scientific Research Fund Grant No. OTKA/K-120356 to AS and AT.
2024-04-222024-04-222024-07-04Bibliographically approved