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Sökning: id:"swepub:oai:DiVA.org:uu-212076" > A Model for Mild Tr...

A Model for Mild Traumatic Brain Injury that Induces Limited Transient Memory Impairment and Increased Levels of Axon Related Serum Biomarkers

Rostami, Elham, 1979- (författare)
Karolinska Institutet
Davidsson, Johan, 1967 (författare)
Chalmers tekniska högskola,Chalmers University of Technology
Ng, Kian Chye (författare)
DSO National Laboratories
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Lu, Jia (författare)
DSO National Laboratories
Gyorgy, Andrea (författare)
Uniformed Services University of the Health Sciences
Walker, Johan (författare)
Uniformed Services University of the Health Sciences
Wingo, Daniel (författare)
Uniformed Services University of the Health Sciences
Plantman, Stefan (författare)
Karolinska Institutet
Bellander, Bo-Michael (författare)
Karolinska Institutet
Agoston, Denes V. (författare)
Uniformed Services University of the Health Sciences
Risling, Mårten (författare)
Karolinska Institutet
Angeria, Maria (författare)
Karolinska Institutet
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 (creator_code:org_t)
2012
2012
Engelska.
Ingår i: Frontiers in Neurology. - : Frontiers Media SA. - 1664-2295. ; 3, s. 115-
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Mild traumatic brain injury (mTBI) is one of the most common neuronal insults and can lead to long-term disabilities. mTBI occurs when the head is exposed to a rapid acceleration-deceleration movement triggering axonal injuries. Our limited understanding of the underlying pathological changes makes it difficult to predict the outcome of mTBI. In this study we used a scalable rat model for rotational acceleration TBI, previously characterized for the threshold of axonal pathology. We have analyzed whether a TBI just above the defined threshold would induce any detectable behavioral changes and/or changes in serum biomarkers. The effect of injury on sensory motor functions, memory and anxiety were assessed by beam walking, radial arms maze and elevated plus maze at 3–7 days following TBI. The only behavioral deficits found were transient impairments in working and reference memory. Blood serum was analyzed at 1, 3, and 14 days after injury for changes in selected protein biomarkers. Serum levels of neurofilament heavy chain and Tau, as well as S100B and myelin basic protein showed significant increases in the injured animals at all time points. No signs of macroscopic injuries such as intracerebral hematomas or contusions were found. Amyloid precursor protein immunostaining indicated axonal injuries at all time points analyzed. In summary, this model mimics some of the key symptoms of mTBI, such as transient memory impairment, which is paralleled by an increase in serum biomarkers. Our findings suggest that serum biomarkers may be used to detect mTBI. The model provides a suitable foundation for further investigation of the underlying pathology of mTBI.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)
NATURVETENSKAP  -- Annan naturvetenskap (hsv//swe)
NATURAL SCIENCES  -- Other Natural Sciences (hsv//eng)

Nyckelord

Diffuse axona injury
Traumatic brain injury
APP
DAI
S100B
serum biomarker
Brain trauma model
Neurosurgery
Neurokirurgi
Neuroscience
Neurovetenskap

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