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  • Laitera, TiinaUniv Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland.;Univ Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland. (author)

The Expression of Transthyretin and Amyloid-beta Protein Precursor is Altered in the Brain of Idiopathic Normal Pressure Hydrocephalus Patients

  • Article/chapterEnglish2015

Publisher, publication year, extent ...

  • 2015
  • printrdacarrier

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  • LIBRIS-ID:oai:DiVA.org:uu-268725
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-268725URI
  • https://doi.org/10.3233/JAD-150268DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Happasalo, Hiltunen och Leinonen bidrog i lika stor utsträckning till artikeln.
  • Background: Idiopathic normal pressure hydrocephalus (iNPH) is a dementing condition in which Alzheimer's disease (AD)related amyloid-beta (A beta) plaques are frequently observed in the neocortex. iNPH patients with prominent A beta pathology show AD-related alterations in amyloid-beta protein precursor (A beta PP) processing resulting from increased gamma-secretase activity. Objectives: Our goal was to assess potential alterations in the global gene expression profile in the brain of iNPH patients as compared to non-demented controls and to evaluate the levels of the identified targets in the cerebrospinal fluid (CSF) of iNPH patients. Methods: The genome-wide expression profile of similar to 35,000 probes was assessed in the RNA samples obtained from 22 iNPH patients and eight non-demented control subjects using a microarray chip. The soluble levels of sA beta PP alpha, sA beta PP beta, and transthyretin (TTR) were measured from the CSF of 102 iNPH patients using ELISA. Results: After correcting the results for multiple testing, significant differences in the expression of TTR and A beta PP were observed between iNPH and control subjects. The mRNA levels of TTR were on average 17-fold lower in iNPH samples compared to control samples. Conversely, the expression level of A beta PP was on average three times higher in iNPH samples as compared to control samples. Interestingly, the expression of beta-secretase (ADAM10) was also increased in iNPH patients. In the lumbar CSF samples, soluble TTR levels showed a significant positive correlation with sA beta PP alpha and sA beta PP beta, but TTR levels did not predict the brain pathology or the shunt response. Conclusions: These findings suggest differences in the expression profile of key factors involved in AD-related cellular events in the brain of iNPH patients.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Kurki, Mitja I.Univ Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland. (author)
  • Pursiheimo, Juha-PekkaUniv Turku, Inst Biomed, Turku, Finland. (author)
  • Zetterberg, HenrikUniv Gothenburg, Sahlgrenska Acad, Clin Neurochem Lab, Dept Psychiat & Neurochem, Gothenburg, Sweden. (author)
  • Helisalmi, SeppoUniv Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland. (author)
  • Rauramaa, TuomasUniv Eastern Finland, Inst Clin Med Pathol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Pathol, SF-70210 Kuopio, Finland. (author)
  • Alafuzoff, IrinaUppsala universitet,Institutionen för immunologi, genetik och patologi(Swepub:uu)irial548 (author)
  • Remes, Anne M.Univ Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland. (author)
  • Soininen, HilkkaUniv Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland. (author)
  • Haapasalo, AnnakaisaUniv Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland.;AI Virtanen Inst Mol Sci, Dept Neurobiol, Kuopio, Finland. (author)
  • Jaaskelainen, Juha E.Univ Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland. (author)
  • Hiltunen, MikkoUniv Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland.;Univ Eastern Finland, Inst Biomed, Kuopio, Finland. (author)
  • Leinonen, VilleUniv Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland. (author)
  • Univ Eastern Finland, Inst Clin Med Neurol, Kuopio, Finland.;Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland.;Univ Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland.Univ Eastern Finland, Inst Clin Med Neurosurg, Kuopio, Finland.;Kuopio Univ Hosp, Neurosurg NeuroCtr, SF-70210 Kuopio, Finland. (creator_code:org_t)

Related titles

  • In:Journal of Alzheimer's Disease48:4, s. 959-9681387-28771875-8908

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