umu.sePublikationer
Ändra sökning
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Brain parenchymal fraction in healthy adults: a systematic review of the literature
Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Klinisk neurovetenskap.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Klinisk neurovetenskap. Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
2017 (Engelska)Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, nr 1, artikel-id e0170018Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Brain atrophy is an important feature of many neurodegenerative disorders. It can be described in terms of change in the brain parenchymal fraction (BPF). In order to interpret the BPF in disease, knowledge on the BPF in healthy individuals is required. The aim of this study was to determine data on the BPF of healthy individuals via a systematic review of the literature. The databases PubMed and Scopus were searched and 95 articles, including a total of 9269 individuals, were identified including the required data. We present values of BPF from healthy individuals stratified by age and post-processing method. The BPF correlated with age and there were significant differences in age-adjusted BPF between methods. This study contributes to increased knowledge on BPF in healthy individuals, which may assist in the interpretation of BPF in the setting of disease. We highlight the differences between post-processing methods and the need for a consensus gold standard. 

Ort, förlag, år, upplaga, sidor
2017. Vol. 12, nr 1, artikel-id e0170018
Nationell ämneskategori
Neurologi
Identifikatorer
URN: urn:nbn:se:umu:diva-128695DOI: 10.1371/journal.pone.0170018ISI: 000392372300051PubMedID: 28095463OAI: oai:DiVA.org:umu-128695DiVA, id: diva2:1055538
Tillgänglig från: 2016-12-12 Skapad: 2016-12-12 Senast uppdaterad: 2018-06-09Bibliografiskt granskad
Ingår i avhandling
1. Brain parenchymal fraction in healthy individuals and in clinical follow-up of multiple sclerosis
Öppna denna publikation i ny flik eller fönster >>Brain parenchymal fraction in healthy individuals and in clinical follow-up of multiple sclerosis
2016 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Background Multiple sclerosis (MS) is an autoimmune disease characterised by inflammatory damage to the central nervous system (CNS). Accumulated CNS injury can be quantified as brain atrophy, definable as a reduction in brain parenchymal fraction (BPF). BPF correlate with disability in MS and is used routinely as an endpoint in clinical trials. In 2009/2010, a new MS clinical care program, that includes follow-up of BPF, was introduced at Umeå University Hospital (NUS). Levels of neurofilament light polypetide (NFL) and glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) are markers of axonal and astrocytic injury, respectively, and also potential surrogate biomarkers for BPF decline. The goals of this thesis were to establish age-adjusted values of BPF in healthy individuals and to relate these to the BPF values from individuals with MS as well as to the levels of NFL and GFAP in CSF. Another goal was to investigate if expanded disability status scale (EDSS)-worsening could be predicted in a clinical MS cohort and if BPF measurements could contribute to such predictions. Methods A group of 111 healthy individuals volunteered to participate in the studies. A total of 106 of these underwent MRI with BPF measurements, 53 underwent lumbar puncture (LP) with measurement of NFL and GFAP and 48 underwent both MRI and LP. Three different automatic and one manual method were utilised to determine BPF. A literature search on BPF in healthy individuals was performed for the purpose of a systematic review. For studying disability progression in MS, all individuals with MS followed at NUS and included in the Swedish MS registry were included if they had matched data on BPF, EDSS and lesion load as part of clinical follow-up (n=278). Results BPF as well as NFL and GFAP levels in CSF were all associated with age. NFL was associated with BPF and GFAP, but only the association with GFAP was retained when adjusting for age. Significant differences were found between different methods for BPF determination. In the MS population, BPF was associated with EDSS. Only progressive disease course could predict EDSS worsening. Conclusion The data on BPF and levels of NFL and GFAP in CSF of healthy individuals can aid in the interpretation of these variables in the setting of MS. Knowledge on differences in BPF data from different methods for BPF determination can be useful in comparing data across studies, but also highlights the need for a commonly accepted gold standard. The correlation between GFAP and NFL levels in CSF may indicate an association between glial and axonal turnover that is independent of the aging effect on the brain. However, the low number of volunteers for LP precluded clear conclusions. An association between BPF and EDSS was seen in the MS group. The ability to predict EDSS worsening in the clinical MS cohort was limited.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå universitet, 2016. s. 80
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1867
Nyckelord
Brain parenchymal fraction, Neurofilament light, Glial fibrillary acidic protein, Brain atrophy, Multiple Sclerosis, Clinical follow-up
Nationell ämneskategori
Neurologi
Identifikatorer
urn:nbn:se:umu:diva-128697 (URN)978-91-7601-621-3 (ISBN)
Disputation
2017-01-20, Sal A, Tandläkarhögskolan 9 trappor, byggnad 1D, Umeå, 13:00 (Svenska)
Opponent
Handledare
Tillgänglig från: 2016-12-16 Skapad: 2016-12-12 Senast uppdaterad: 2018-06-09Bibliografiskt granskad

Open Access i DiVA

fulltext(2687 kB)131 nedladdningar
Filinformation
Filnamn FULLTEXT01.pdfFilstorlek 2687 kBChecksumma SHA-512
0efc67d267f29ab506b702518fb4dfff47db5178e0d57797f6e32a5556eb5bcfc1ff22d99896ee81746b51ba2f8539cdf866c1870ee336d87bc9f48ee866b620
Typ fulltextMimetyp application/pdf

Övriga länkar

Förlagets fulltextPubMed

Personposter BETA

Vågberg, MattiasGranåsen, GabrielSvenningsson, Anders

Sök vidare i DiVA

Av författaren/redaktören
Vågberg, MattiasGranåsen, GabrielSvenningsson, Anders
Av organisationen
Klinisk neurovetenskapEpidemiologi och global hälsa
I samma tidskrift
PLoS ONE
Neurologi

Sök vidare utanför DiVA

GoogleGoogle Scholar
Totalt: 131 nedladdningar
Antalet nedladdningar är summan av nedladdningar för alla fulltexter. Det kan inkludera t.ex tidigare versioner som nu inte längre är tillgängliga.

doi
pubmed
urn-nbn

Altmetricpoäng

doi
pubmed
urn-nbn
Totalt: 265 träffar
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf