The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease.
Open accessAbstract
In a recent preliminary study it was reported that a severe head injury resulted in the deposition of beta amyloid protein (beta AP) in the cortical ribbon of 30% of patients who survived for less than two weeks. Multiple cortical areas have now been examined from 152 patients (age range 8 weeks-81 years) after a severe head injury with a survival time of between four hours and 2.5 years. This series was compared with a group of 44 neurologically normal controls (age range 51 to 80 years). Immunostaining with an antibody to beta AP confirmed the original findings that 30% of cases of head injury have beta AP deposits in one or more cortical areas. Increasing age seemed to accentuate the extent of beta AP deposition and potential correlations with other pathological changes associated with head injury were also investigated. In addition, beta amyloid precursor protein (beta APP) immunoreactivity was increased in the perikarya of neurons in the vicinity of beta AP deposits. The data from this study support proposals that increased expression of beta APP is part of an acute phase response to neuronal injury in the human brain, that extensive overexpression of beta APP can lead to deposition of beta AP and the initiation of an Alzheimer disease-type process within days, and that head injury may be an important aetiological factor in Alzheimer's disease.
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“The rapid accumulation of Aβ after TBI is well documented in both humans and experimental animal models.12–17”
From Controlled Cortical Impact Results in an Extensive Loss of Dendritic Spines that Is Not Mediated by Injury-Induced Amyloid-Beta Accumulation (2013) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Third, accumulation of APP and extracellular deposition of the 40- to 42-amino acid Aβ peptide in senile plaques has been identified in human brain tissue soon after severe TBI (29, 30).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Clinical studies indicate that Aβ accumulates within hours after severe TBI and is spread throughout the cerebral cortex compared to age-matched controls (29, 31).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The co-occurrence of TBI and APP mutation in the clinical setting is rare (29) thereby restricting the results of many of these studies.”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [29]
Experimental — accuracy not yet measuredIn the citing paper
“a rapid generation and deposition of Aβ in stroke and after head trauma, which could benefit to maintain the BBB integrity and inhibit the leakage of serum components into the brain, leading to neuroinflammation.436”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [436]
In the citing paper
“Individuals, including children, who died following coma not long after severe head trauma were shown to develop amorphous cerebral Aβ plaques [152].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [152]
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Cites
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Research works printed but not linked: 3
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Metadata
- Authors
- Roberts, G. W., Gentleman, S. M., Lynch, A., Murray, L., Landon, M., & Graham, D. I.
- Venue
- Journal of Neurology, Neurosurgery & Psychiatry
- Publisher
- BMJ
- Published
- 1994-04-01
- Volume
- 57
- Issue
- 4
- Pages
- 419-425
- ISSN
- 0022-3050 (ISSN-L)
- PMC
- PMC1072869
- OpenAlex
- W2073009405
- Cited by
- 569
- References
- 42
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 22 · 2021: 22 · 2020: 18 · 2019: 28 · 2018: 18 · 2017: 21 · 2016: 29 · 2015: 31 · 2014: 20 · 2013: 28 · 2012: 26
- FWCI
- 11.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurology Neurosurgery & Psychiatry (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- severe traumatic brain injury, traumatic brain injury, Alzheimer's disease pathogenesis, amyloid precursor protein, immunostaining
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Brain Injuries, Child, Child, Preschool, Female, Humans, Immunohistochemistry, Infant, Male, Middle Aged, Amyloid beta-Peptides
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