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Rapid amyloid-β oli...
Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury
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- Abu Hamdeh, Sami (författare)
- Uppsala universitet,Neurokirurgi
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- Rollman Waara, Erik (författare)
- BioArctic Neurosci AB, Stockholm, Sweden
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- Möller, Christer (författare)
- BioArctic Neurosci AB, Stockholm, Sweden
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- Söderberg, Linda (författare)
- BioArctic Neurosci AB, Stockholm, Sweden
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- Basun, Hans (författare)
- Uppsala universitet,Geriatrik,BioArctic Neuroscience AB, Stockholm, Sweden
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- Alafuzoff, Irina (författare)
- Uppsala universitet,Klinisk och experimentell patologi
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- Hillered, Lars, 1952- (författare)
- Uppsala universitet,Neurokirurgi
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- Lannfelt, Lars (författare)
- Uppsala universitet,Geriatrik,BioArctic Neuroscience AB, Stockholm, Sweden
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- Ingelsson, Martin (författare)
- Uppsala universitet,Geriatrik
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- Marklund, Niklas (författare)
- Uppsala universitet,Neurokirurgi
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(creator_code:org_t)
- 2017-06-19
- 2018
- Engelska.
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Ingår i: Brain Pathology. - : Wiley. - 1015-6305 .- 1750-3639. ; 28:4, s. 451-462
- Relaterad länk:
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https://www.ncbi.nlm...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Deposition of amyloid-β (Aβ) is central to Alzheimer's disease (AD) pathogenesis and associated with progressive neurodegeneration in traumatic brain injury (TBI). We analyzed predisposing factors for Aβ deposition including monomeric Aβ40, Aβ42 and Aβ oligomers/protofibrils, Aβ species with pronounced neurotoxic properties, following human TBI. Highly selective ELISAs were used to analyze N-terminally intact and truncated Aβ40 and Aβ42, as well as Aβ oligomers/protofibrils, in human brain tissue, surgically resected from severe TBI patients (n = 12; mean age 49.5 ± 19 years) due to life-threatening brain swelling/hemorrhage within one week post-injury. The TBI tissues were compared to post-mortem AD brains (n = 5), to post-mortem tissue of neurologically intact (NI) subjects (n = 4) and to cortical biopsies obtained at surgery for idiopathic normal pressure hydrocephalus patients (iNPH; n = 4). The levels of Aβ40 and Aβ42 were not elevated by TBI. The levels of Aβ oligomers/protofibrils in TBI were similar to those in the significantly older AD patients and increased compared to NI and iNPH controls (P < 0.05). Moreover, TBI patients carrying the AD risk genotype Apolipoprotein E epsilon3/4 (APOE ε3/4; n = 4) had increased levels of Aβ oligomers/protofibrils (P < 0.05) and of both N-terminally intact and truncated Aβ42 (P < 0.05) compared to APOE ε3/4-negative TBI patients (n = 8). Neuropathological analysis showed insoluble Aβ aggregates (commonly referred to as Aβ plaques) in three TBI patients, all of whom were APOE ε3/4 carriers. We conclude that soluble intermediary Aβ aggregates form rapidly after TBI, especially among APOE ε3/4 carriers. Further research is needed to determine whether these aggregates aggravate the clinical short- and long-term outcome in TBI.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Neurosciences (hsv//eng)
Nyckelord
- Alzheimer's disease
- amyloid β oligomers
- amyloid-β
- traumatic brain injury
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Abu Hamdeh, Sami
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Rollman Waara, E ...
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Möller, Christer
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Söderberg, Linda
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Basun, Hans
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Alafuzoff, Irina
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visa fler...
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Hillered, Lars, ...
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Lannfelt, Lars
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Ingelsson, Marti ...
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Marklund, Niklas
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visa färre...
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Brain Pathology
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Uppsala universitet