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| 32. |
- Blennow, Kaj, 1958, et al.
(författare)
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Fluid biomarkers in Alzheimer disease.
- 2012
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Ingår i: Cold Spring Harbor perspectives in medicine. - : Cold Spring Harbor Laboratory. - 2157-1422. ; 2:9
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Tidskriftsartikel (refereegranskat)abstract
- Research progress has provided detailed understanding of the molecular pathogenesis of Alzheimer disease (AD). This knowledge has been translated into new drug candidates with putative disease-modifying effects, which are now being tested in clinical trials. The promise of effective therapy has created a great need for biomarkers able to detect AD in the predementia phase, because drugs will probably be effective only if neurodegeneration is not too advanced. In this chapter, cerebrospinal fluid (CSF) and plasma biomarkers are reviewed. The core CSF biomarkers total tau (T-tau), phosphorylated tau (P-tau) and the 42 amino acid form of β-amyloid (Aβ42) reflect AD pathology, and have high diagnostic accuracy to diagnose AD with dementia and prodromal AD in mild cognitive impairment cases. The rationale for the use of CSF biomarkers to identify and monitor the mechanism of action of new drug candidates is also outlined in this chapter.
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| 33. |
- Blennow, Kaj, 1958, et al.
(författare)
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Fluid Biomarkers in Alzheimer Disease, 91
- 2012
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Ingår i: The biology of Alzheimer disease / edited by Dennis J. Selkoe, David M. Holtzman, and Eckhard Mandelkow.. - Cold Spring Harbor, N.Y. : Cold Spring Harbor Laboratory Press. - 9781936113446 ; , s. 91-114
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Bokkapitel (refereegranskat)
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| 34. |
- Blennow, Kaj, 1958, et al.
(författare)
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Is it time for biomarker-based diagnostic criteria for prodromal Alzheimer's disease?
- 2010
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Ingår i: Alzheimer's research & therapy. - : Springer Science and Business Media LLC. - 1758-9193. ; 2:2
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Forskningsöversikt (refereegranskat)abstract
- ABSTRACT: Drug candidates targeting amyloid-beta (Abeta) pathology in Alzheimer's disease are in different phases of clinical trials. These treatments will probably be most effective in the earlier stages of the disease, before neurodegeneration is too severe, but at the same time symptoms are vague and the clinical diagnosis is difficult. Recent research advances have resulted in promising biomarkers, including cerebrospinal fluid analyses for tau and Abeta, magnetic resonance imaging measurement of atrophy, and positron emission tomography imaging of glucose metabolism and Abeta pathology, which allow identification of prodromal Alzheimer's disease. More details are needed, however, on how these biomarkers can be standardized, to allow a general implementation in the clinical routine diagnostic work-up of patients with cognitive disturbances.
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| 35. |
- Blennow, Kaj, 1958, et al.
(författare)
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Likvoranalyser : Del av: Sjukdomar i centrala nervsystemet
- 2012
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Ingår i: Laurells Klinisk kemi i praktisk medicin 9., [rev. och utök.] uppl. /redaktion: Peter Nilsson-Ehle, Maria Berggren Söderlund, Elvar Theodorsson ; redaktionskommitté: Charlotte Becker, Kjell Grankvist, Anders Grubb, Göran Lindstedt, Per Simonsson. - LUND : Studentlitteratur. - 9789144047874
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 38. |
- Blennow, Kaj, 1958, et al.
(författare)
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No neurochemical evidence of brain injury after blast overpressure by repeated explosions or firing heavy weapons.
- 2011
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Ingår i: Acta neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 123, s. 245-51
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Tidskriftsartikel (refereegranskat)abstract
- Blennow K, Jonsson M, Andreasen N, Rosengren L, Wallin A, Hellström PA, Zetterberg H. No neurochemical evidence of brain injury after blast overpressure by repeated explosions or firing heavy weapons.Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01408.x .(c) 2010 John Wiley & Sons A/S. Background - Psychiatric and neurological symptoms are common among soldiers exposed to blast without suffering a direct head injury. It is not known whether such symptoms are direct consequences of blast overpressure. Objective - To examine if repeated detonating explosions or firing if of heavy weapons is associated with neurochemical evidence of brain damage. Materials and methods - Three controlled experimental studies. In the first, army officers were exposed to repeated firing of a FH77B howitzer or a bazooka. Cerebrospinal fluid (CSF) was taken post-exposure to measure biomarkers for brain damage. In the second, officers were exposed for up to 150 blasts by firing a bazooka, and in the third to 100 charges of detonating explosives of 180 dB. Serial serum samples were taken after exposure. Results were compared with a control group consisting of 19 unexposed age-matched healthy volunteers. Results - The CSF biomarkers for neuronal/axonal damage (tau and neurofilament protein), glial cell injury (GFAP and S-100b), blood-brain barrier damage (CSF/serum albumin ratio) and hemorrhages (hemoglobin and bilirubin) and the serum GFAP and S-100b showed normal and stable levels in all exposed officers. Discussion - Repeated exposure to high-impact blast does not result in any neurochemical evidence of brain damage. These findings are of importance for soldiers regularly exposed to high-impact blast when firing artillery shells or other types of heavy weapons.
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