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(WFRF:(Overvad Kim)) pers:(Spijkerman Annemieke M. W.)
 

Search: (WFRF:(Overvad Kim)) pers:(Spijkerman Annemieke M. W.) > (2014) > Amyloid pathology a...

Amyloid pathology and axonal injury after brain trauma

Scott, G. (author)
Ramlackhansingh, A. F. (author)
Edison, P. (author)
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Hellyer, P. (author)
Cole, J. (author)
Veronese, M. (author)
Leech, R. (author)
Greenwood, R. J. (author)
Turkheimer, F. E. (author)
Gentleman, S. M. (author)
Heckemann, Rolf A. (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
Matthews, P. M. (author)
Brooks, D. J. (author)
Sharp, D. J. (author)
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 (creator_code:org_t)
2016-02-03
2016
English.
In: Neurology. - : Ovid Technologies (Wolters Kluwer Health). - 0028-3878 .- 1526-632X. ; 86:9, s. 821-828
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Objective:To image -amyloid (A) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and A are correlated, and compare the spatial distribution of A to Alzheimer disease (AD).Methods:Patients 11 months to 17 years after moderate-severe TBI underwent C-11-Pittsburgh compound B (C-11-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BPND) images of C-11-PiB, which index A plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy, was estimated and correlated with C-11-PiB BP(ND.)Results:Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased C-11-PiB BPND was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy of associated white matter tracts and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum.Conclusions:Increased A burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathologic features of dementia, which may relate to axonal damage produced by the injury.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

Keyword

alzheimers-disease
dementia
network
registration
dysfunction
progression
deposition
severity
anatomy
atrophy
Neurosciences & Neurology

Publication and Content Type

ref (subject category)
art (subject category)

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