Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?
Open accessAbstract
Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI.
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Diffuse Aβ plaques can be detected in brain of 30% of individuals that acutely die from TBI.
“Interestingly, diffuse Aβ plaques can be detected in the brain of 30% of individuals that acutely die from TBI.89”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [89]
In “Human TBI and Aβ plaques,” the review says plaques are found in up to 30% of patients who die acutely following TBI, and that the plaques are typically diffuse. The citing sentence omits “up to,” making 30% sound like a fixed rate rather than an upper bound. (LLM, conf=0.83)
Experimental — accuracy not yet measuredSeveral lines of evidence point to a relationship between single-incident TBI and AD.
“Several lines of evidence point to a relationship between single-incident TBI and AD (10, 11).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [10]
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Traumatic Brain Injury as a Trigger of Neurodegeneration
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- Authors
- Johnson, V. E., Stewart, W., & Smith, D. H.
- Affiliations
- University of Glasgow (GB)
- University of Pennsylvania Health System (US)
- Corresponding author
- Smith, Douglas H.
- Venue
- Nature Reviews Neuroscience
- Published
- 2010-03-10
- Volume
- 11
- Issue
- 5
- Pages
- 361-370
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC3979339
- OpenAlex
- W2023819682
- Cited by
- 587
- References
- 184
- Citations by year
- 2026: 26 · 2025: 44 · 2024: 30 · 2023: 41 · 2022: 27 · 2021: 47 · 2020: 48 · 2019: 47 · 2018: 45 · 2017: 33 · 2016: 42 · 2015: 32 · 2014: 28 · 2013: 37 · 2012: 35
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS-038104, R01NS038104, P01NS056202, NS 056202)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, Alzheimer's disease, amyloid-beta, amyloid plaques, axonal injury, amyloid precursor protein, neurodegeneration
- MeSH terms
- Alzheimer Disease, Axons, Brain, Brain Injuries, Humans, Amyloid beta-Peptides, Plaque, Amyloid
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