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Amyloid-beta and Ta...
Amyloid-beta and Tau Dynamics in Human Brain Interstitial Fluid in Patients with Suspected Normal Pressure Hydrocephalus
- Article/chapterEnglish2015
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LIBRIS-ID:oai:gup.ub.gu.se/218710
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https://gup.ub.gu.se/publication/218710URI
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https://doi.org/10.3233/jad-142862DOI
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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Background: Amyloid-beta (A beta(1-42)), total tau (T-tau), and phosphorylated tau (P-tau(181)) in the cerebrospinal fluid (CSF) are the most promising biomarkers of Alzheimer's disease (AD). Still, little is known about the dynamics of these molecules in the living brain. In a transgenic mouse brain, soluble A beta decreases with increasing age and advanced A beta pathology as seen similarly in CSF. Objective: To assess the relationship between AD-related pathological changes in human brain tissue, ventricular and lumbar CSF, and brain interstitial fluid (ISF). Methods: Altogether 11 patients with suspected idiopathic normal pressure hydrocephalus underwent frontal cortical brain biopsy, 24-h intraventricular pressure monitoring, and a microdialysis procedure. AD-related biomarkers were analyzed from brain tissue, CSF, and ISF. Results: ISF T-tau levels decreased strongly within the first 12 h, then plateauing until the end of the experiment. A beta(1-42) and P-tau(181) remained stable during the experiment (n = 3). T-tau and P-tau were higher in the ISF than in ventricular or lumbar CSF, while A beta(1-42) levels were within similar range in both CSF and ISF samples. ISF P-tau correlated with the ventricular CSF T-tau (r = 0.70, p = 0.017) and P-tau(181) (r = 0.64, p = 0.034). Five patients with amyloid pathology in the brain biopsy tended to reveal lower ISF A beta(1-42) levels than those six without amyloid pathology. Conclusions: This is the first study to report ISF A beta and tau levels in the human brain without significant brain injury. The set-up used enables sampling from the brain ISF for at least 24 h without causing adverse effects due to the microdialysis procedure to follow the dynamics of the key molecules in AD pathogenesis in the living brain at various stages of the disease.
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Rummukainen, J.
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Ihalainen, J.
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Fraunberg, Mvuz
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Koivisto, A. M.
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Nerg, O.
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Puli, L. K.
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Seppala, T. T.
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Zetterberg, Henrik,1973Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xzethe
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Pyykko, O. T.
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Helisalmi, S.
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Tanila, H.
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Alafuzoff, I.
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Hiltunen, M.
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Rinne, J.
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Soininen, H.
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Jaaskelainen, J. E.
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Leinonen, V.
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Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
(creator_code:org_t)
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In:Journal of Alzheimers Disease: IOS Press46:1, s. 261-2691387-28771875-8908
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Herukka, S. K.
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Rummukainen, J.
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Ihalainen, J.
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Fraunberg, Mvuz
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Koivisto, A. M.
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Nerg, O.
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Puli, L. K.
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Seppala, T. T.
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Zetterberg, Henr ...
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Pyykko, O. T.
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Helisalmi, S.
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Tanila, H.
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Alafuzoff, I.
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Hiltunen, M.
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Rinne, J.
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Soininen, H.
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Jaaskelainen, J. ...
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Leinonen, V.
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- MEDICAL AND HEALTH SCIENCES
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and Basic Medicine
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and Neurosciences
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University of Gothenburg