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Cerebrospinal fluid...
Cerebrospinal fluid-induced retardation of amyloid β aggregation correlates with Alzheimer's disease and the APOE ε4 allele
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- Padayachee, E. R. (författare)
- University of Gothenburg
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- Zetterberg, H. (författare)
- University of Gothenburg,University College London
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- Portelius, E. (författare)
- University of Gothenburg
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- Borén, J. (författare)
- University of Gothenburg
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- Molinuevo, J. L. (författare)
- Hospital Clínic of Barcelona
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- Andreasen, N. (författare)
- Karolinska University Hospital
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- Cukalevski, R. (författare)
- Lund University,Lunds universitet,Biokemi och Strukturbiologi,Centrum för Molekylär Proteinvetenskap,Kemiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Biochemistry and Structural Biology,Center for Molecular Protein Science,Department of Chemistry,Departments at LTH,Faculty of Engineering, LTH
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- Linse, S. (författare)
- Lund University,Lunds universitet,Biokemi och Strukturbiologi,Centrum för Molekylär Proteinvetenskap,Kemiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Biochemistry and Structural Biology,Center for Molecular Protein Science,Department of Chemistry,Departments at LTH,Faculty of Engineering, LTH
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- Blennow, K. (författare)
- University of Gothenburg
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- Andreasson, U. (författare)
- University of Gothenburg
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(creator_code:org_t)
- Elsevier BV, 2016
- 2016
- Engelska 6 s.
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Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 1651, s. 11-16
- Relaterad länk:
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http://dx.doi.org/10... (free)
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https://doi.org/10.1...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Misfolding and aggregation of amyloid β (Aβ) are key features of Alzheimer's disease (AD) pathogenesis, but the molecular events controlling this process are not known in detail. In vivo, Aβ aggregation and plaque formation occur in the interstitial fluid of the brain extracellular matrix. This fluid communicates freely with cerebrospinal fluid (CSF). Here, we examined the effect of human CSF on Aβ aggregation kinetics in relation to AD diagnosis and carrier status of the apolipoprotein E (APOE) ε4 allele, the main genetic risk factor for sporadic AD. The aggregation of Aβ was inhibited in the presence of CSF and, surprisingly, the effect was more pronounced in APOE ε4 carriers. However, by fractionation of CSF using size exclusion chromatography, it became evident that it was not the ApoE protein itself that conveyed the inhibition, since the retarding species eluted at lower volume, corresponding to a much higher molecular weight, than ApoE monomers. Cholesterol quantification and immunoblotting identified high-density lipoprotein particles in the retarding fractions, indicating that such particles may be responsible for the inhibition. These results add information to the yet unresolved puzzle on how the risk factor of APOE ε4 functions in AD pathogenesis.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Neurologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Neurology (hsv//eng)
Nyckelord
- Aggregation
- Amyloid-β
- Apolipoprotein ε4
- Cholesterol
- High density lipoproteins
- Inhibition
- Kinetics
- Neurofibrillary tangles
- Thioflavin T
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
Hitta via bibliotek
Till lärosätets databas
- Av författaren/redakt...
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Padayachee, E. R ...
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Zetterberg, H.
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Portelius, E.
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Borén, J.
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Molinuevo, J. L.
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Andreasen, N.
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visa fler...
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Cukalevski, R.
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Linse, S.
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Blennow, K.
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Andreasson, U.
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visa färre...
- Om ämnet
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- MEDICIN OCH HÄLSOVETENSKAP
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MEDICIN OCH HÄLS ...
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och Klinisk medicin
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och Neurologi
- Artiklar i publikationen
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Brain Research
- Av lärosätet
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Lunds universitet