Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions
We aimed to detect the possible accelerating role of previous traumatic brain injury (TBI) exposures on the onset of later cognitive decline assessed across different brain diseases. We analyzed data from the National Alzheimer's Coordinating Center (NACC), which provide information on history...
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| Language: | English |
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Frontiers Media S.A.
2021-05-01
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| Series: | Frontiers in Neurology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fneur.2021.573401/full |
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| author | Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Sorana Raiciulescu Cara Olsen Daniel P. Perl Daniel P. Perl |
| author_facet | Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Sorana Raiciulescu Cara Olsen Daniel P. Perl Daniel P. Perl |
| author_sort | Diego Iacono |
| collection | DOAJ |
| description | We aimed to detect the possible accelerating role of previous traumatic brain injury (TBI) exposures on the onset of later cognitive decline assessed across different brain diseases. We analyzed data from the National Alzheimer's Coordinating Center (NACC), which provide information on history of TBI and longitudinal data on cognitive and non-cognitive domains for each available subject. At the time of this investigation, a total of 609 NACC subjects resulted to have a documented history of TBI. We compared subjects with and without a history of previous TBI (of any type) at the time of their first cognitive decline assessment, and termed them, respectively, TBI+ and TBI– subjects. Three hundred and sixty-one TBI+ subjects (229 male/132 female) and 248 TBI– subjects (156 male/92 female) were available. The analyses included TBI+ and TBI– subjects with a clinical diagnosis of Mild Cognitive Impairment, Alzheimer's disease, Dementia with Lewy bodies, Progressive supranuclear palsy, Corticobasal degeneration, Frontotemporal dementia, Vascular dementia, non-AD Impairment, and Parkinson's disease. The data showed that the mean age of TBI+ subjects was lower than TBI– subjects at the time of their first cognitive decline assessment (71.6 ± 11.2 vs. 74.8 ± 9.5 year; p < 0.001). Moreover, the earlier onset of cognitive decline in TBI+ vs. TBI– subjects was independent of sex, race, attained education, APOE genotype, and importantly, clinical diagnoses. As for specific cognitive aspects, MMSE, Trail Making Test part B and WAIS-R scores did not differ between TBI+ and TBI– subjects, whereas Trail Making Test part A (p = 0.013) and Boston Naming test (p = 0.008) did. In addition, data showed that neuropsychiatric symptoms [based on Neuropsychiatry Inventory (NPI)] were much more frequent in TBI+ vs. TBI– subjects, including AD and non-AD neurodegenerative conditions such as PD. These cross-sectional analyses outcomes from longitudinally-assessed cohorts of TBI+ subjects that is, subjects with TBI exposure before the onset of cognitive decline in the contest of different neurodegenerative disorders and associated pathogenetic mechanisms, are novel, and indicate that a previous TBI exposure may act as a significant “age-lowering” factor on the onset of cognitive decline in either AD and non-AD conditions independently of demographic factors, education, APOE genotype, and current or upcoming clinical conditions. |
| first_indexed | 2024-12-19T23:43:42Z |
| format | Article |
| id | doaj.art-a69b16622368400eb763e920ecf1a197 |
| institution | Directory Open Access Journal |
| issn | 1664-2295 |
| language | English |
| last_indexed | 2024-12-19T23:43:42Z |
| publishDate | 2021-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neurology |
| spelling | doaj.art-a69b16622368400eb763e920ecf1a1972022-12-21T20:01:21ZengFrontiers Media S.A.Frontiers in Neurology1664-22952021-05-011210.3389/fneur.2021.573401573401Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD ConditionsDiego Iacono0Diego Iacono1Diego Iacono2Diego Iacono3Diego Iacono4Diego Iacono5Sorana Raiciulescu6Cara Olsen7Daniel P. Perl8Daniel P. Perl9Department of Defense/Uniformed Services University (DoD/USU) Brain Tissue Repository & Neuropathology Program, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesDepartment of Neurology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesDepartment of Pathology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesNeuroscience Graduate Program, Department of Anatomy, Physiology, and Genetics, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesThe Henry M. Jackson Foundation for the Advancement of Military Medicine (HJF), Bethesda, MD, United StatesComplex Neurodegenerative Disorders, Neurodegenerative Disorders Clinic, National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda, MD, United StatesDepartment of Preventive Medicine and Biostatistics, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesDepartment of Preventive Medicine and Biostatistics, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesDepartment of Defense/Uniformed Services University (DoD/USU) Brain Tissue Repository & Neuropathology Program, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesDepartment of Pathology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Science (USU), Bethesda, MD, United StatesWe aimed to detect the possible accelerating role of previous traumatic brain injury (TBI) exposures on the onset of later cognitive decline assessed across different brain diseases. We analyzed data from the National Alzheimer's Coordinating Center (NACC), which provide information on history of TBI and longitudinal data on cognitive and non-cognitive domains for each available subject. At the time of this investigation, a total of 609 NACC subjects resulted to have a documented history of TBI. We compared subjects with and without a history of previous TBI (of any type) at the time of their first cognitive decline assessment, and termed them, respectively, TBI+ and TBI– subjects. Three hundred and sixty-one TBI+ subjects (229 male/132 female) and 248 TBI– subjects (156 male/92 female) were available. The analyses included TBI+ and TBI– subjects with a clinical diagnosis of Mild Cognitive Impairment, Alzheimer's disease, Dementia with Lewy bodies, Progressive supranuclear palsy, Corticobasal degeneration, Frontotemporal dementia, Vascular dementia, non-AD Impairment, and Parkinson's disease. The data showed that the mean age of TBI+ subjects was lower than TBI– subjects at the time of their first cognitive decline assessment (71.6 ± 11.2 vs. 74.8 ± 9.5 year; p < 0.001). Moreover, the earlier onset of cognitive decline in TBI+ vs. TBI– subjects was independent of sex, race, attained education, APOE genotype, and importantly, clinical diagnoses. As for specific cognitive aspects, MMSE, Trail Making Test part B and WAIS-R scores did not differ between TBI+ and TBI– subjects, whereas Trail Making Test part A (p = 0.013) and Boston Naming test (p = 0.008) did. In addition, data showed that neuropsychiatric symptoms [based on Neuropsychiatry Inventory (NPI)] were much more frequent in TBI+ vs. TBI– subjects, including AD and non-AD neurodegenerative conditions such as PD. These cross-sectional analyses outcomes from longitudinally-assessed cohorts of TBI+ subjects that is, subjects with TBI exposure before the onset of cognitive decline in the contest of different neurodegenerative disorders and associated pathogenetic mechanisms, are novel, and indicate that a previous TBI exposure may act as a significant “age-lowering” factor on the onset of cognitive decline in either AD and non-AD conditions independently of demographic factors, education, APOE genotype, and current or upcoming clinical conditions.https://www.frontiersin.org/articles/10.3389/fneur.2021.573401/fullTBIearlier-onsetneurodegenerative disordersAPOE genotypecognitive decline |
| spellingShingle | Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Diego Iacono Sorana Raiciulescu Cara Olsen Daniel P. Perl Daniel P. Perl Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions Frontiers in Neurology TBI earlier-onset neurodegenerative disorders APOE genotype cognitive decline |
| title | Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions |
| title_full | Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions |
| title_fullStr | Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions |
| title_full_unstemmed | Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions |
| title_short | Traumatic Brain Injury Exposure Lowers Age of Cognitive Decline in AD and Non-AD Conditions |
| title_sort | traumatic brain injury exposure lowers age of cognitive decline in ad and non ad conditions |
| topic | TBI earlier-onset neurodegenerative disorders APOE genotype cognitive decline |
| url | https://www.frontiersin.org/articles/10.3389/fneur.2021.573401/full |
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