The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Enhanced Neurofibrillary Tangle Formation, Cerebral Atrophy, and Cognitive Deficits Induced by Repetitive Mild Brain Injury in a Transgenic Tauopathy Mouse Model
Abstract
Traumatic brain injury (TBI) is a risk factors for Alzheimer's disease (AD), and repetitive TBI (rTBI) may culminate in dementia pugilistica (DP), a syndrome characterized by progressive dementia, parkinsonism, and the hallmark brain lesions of AD, including neurofibrillary tangles (NFTs), formed by abnormal tau filaments and senile plaques (SPs) composed of Abeta fibrils. Previous study showed that mild rTBI (mrTBI) accelerated the deposition of Abeta in the brains of transgenic (Tg) mice (Tg2576) that over-express human Abeta precursor proteins with the familial AD Swedish mutations (APP695swe) and model of AD-like amyloidosis. Here, we report studies of the effects of mrTBI on AD-like tau pathologies in Tg mice expressing the shortest human tau isoform (T44) subjected to mrTBI, causing brain concussion without structural brain damage to simulate injuries linked to DP. Twelve-month-old Tg T44 (n = 18) and wild-type (WT; n = 24) mice were subjected to mrTBI (four times a day, 1 day per week, for 4 weeks; n = 24) or sham treatment (n = 18). Histopathological analysis of mice at 9 months after mrTBI revealed that one of the Tg T44 mice showed extensive telencephalic NFT and cerebral atrophy. Although statistical analysis of neurobehavioral tests at 6 months after mrTBI did not show any significant difference in any of groups of mice, the Tg T44 mouse with extensive NFT had an exceptionally low neurobehavioral score. The reasons for the augmentation of tau pathologies in only o…
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“Similarly, only transgenic tau mouse models [T44 (one mouse), hTau] displayed NFT pathology following repetitive TBI (153, 234).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [234]
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Cites
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Self-citationTau immunohistochemistry in acute brain injury
Smith, C., Graham, D. I., Murray, L. S., & Nicoll, J. A. R. (2003) · Neuropathology and Applied Neurobiology · doi:10.1046/j.1365-2990.2003.00488.x · Cited by 110 · cited 1×
“…clinically by a progressive dementia with parkinsonism, as well as postmortem evidence of abundant senile plaques (SPs) formed by A deposits and neurofibrillary tangles (NFTs) composed of abnormal tau filaments similar to AD (Geddes et al., 1996; Schmidt et al., 2001; Smith et al., 2003).”
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Cited by
Sorted by citations
Chronic impact of traumatic brain injury on outcome and quality of life: a narrative review
Stocchetti, N., & Zanier, E. R. (2016) · Critical Care · doi:10.1186/s13054-016-1318-1 · Cited by 500
“Tau pathology has been shown to occur in rodent models of TBI within 2 weeks of injury [25–27].”
BackgroundNeuropsychology and clinical neuroscience of persistent post-concussive syndrome
Bigler, E. D. (2007) · Journal of the International Neuropsychological Society · doi:10.1017/s135561770808017x · Cited by 445
“Nonetheless, several excellent animal models of concussive injury have recently been established (Gurkoff et al., 2006; Henninger et al., 2005; Milman et al., 2005; Tang et al., 1997; Tashlykov et al., 2007; Ucar et al., 2006; Yoshiyama et al., 2005; Zohar et al., 2003, 2006).”
Alzheimer’s disease and insulin resistance: translating basic science into clinical applications
Felice, F. G. D. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64595 · Cited by 336
Mouzon, B., Chaytow, H., Crynen, G. C., Bachmeier, C. J., Stewart, J., MULLAN, M. J., Stewart, W. B., Jr., & Crawford, F. (2012) · Journal of Neurotrauma · doi:10.1089/neu.2012.2498 · Cited by 298
Tran, H. T., LaFerla, F. M., Holtzman, D. M., & Brody, D. L. (2011) · Journal of Neuroscience · doi:10.1523/jneurosci.0858-11.2011 · Cited by 255
“First, previous TBI models using transgenic mice only used those that overexpress either mutated forms of APP or tau, not both (Smith et al., 1998; Uryu et al., 2002; Yoshiyama et al., 2005).”
Background
Metadata
- Authors
- Yoshiyama, Y., Uryu, K., Higuchi, M., Longhi, L., Hoover, R., Fujimoto, S., McIntosh, T., Lee, V. M.-Y., & Trojanowski, J. Q.
- Affiliations
- University of Pennsylvania (US)
- Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico (IT)
- ORCID
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2005-10
- Volume
- 22
- Issue
- 10
- Pages
- 1134-1141
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- OpenAlex
- W2059869018
- Cited by
- 133
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 9 · 2019: 12 · 2018: 10 · 2017: 8 · 2016: 10 · 2015: 13 · 2014: 11 · 2013: 14 · 2012: 4
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurotrauma (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (P50NS008803, NS P50-08803, NS R01-40978)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- repetitive mild traumatic brain injury, chronic traumatic encephalopathy, neurofibrillary tangles, tau pathology, brain atrophy, cognitive impairment, concussion, Alzheimer's disease, transgenic mouse model, amyloid-beta, amyloid plaques
- MeSH terms
- Animals, Atrophy, Brain Injuries, Cerebral Cortex, Cognition Disorders, Disease Models, Animal, Humans, Immunohistochemistry, Mice, Transgenic, Blotting, Western, Neurofibrillary Tangles, tau Proteins, Maze Learning, Tauopathies, Mice
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