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Neuroinflammation in Lyme neuroborreliosis affects amyloid metabolism

Mattsson, Niklas; Bremell, Daniel; Anckarsater, Rolf; Blennow, Kaj; Anckarsäter, Henrik LU ; Zetterberg, Henrik and Hagberg, Lars (2010) In BMC Neurology 10.
Abstract
Background: The metabolism of amyloid precursor protein (APP) and beta-amyloid (A beta) is widely studied in Alzheimer's disease, where A beta deposition and plaque development are essential components of the pathogenesis. However, the physiological role of amyloid in the adult nervous system remains largely unknown. We have previously found altered cerebral amyloid metabolism in other neuroinflammatory conditions. To further elucidate this, we investigated amyloid metabolism in patients with Lyme neuroborreliosis (LNB). Methods: The first part of the study was a cross-sectional cohort study in 61 patients with acute facial palsy (19 with LNB and 42 with idiopathic facial paresis, Bell's palsy) and 22 healthy controls. CSF was analysed for... (More)
Background: The metabolism of amyloid precursor protein (APP) and beta-amyloid (A beta) is widely studied in Alzheimer's disease, where A beta deposition and plaque development are essential components of the pathogenesis. However, the physiological role of amyloid in the adult nervous system remains largely unknown. We have previously found altered cerebral amyloid metabolism in other neuroinflammatory conditions. To further elucidate this, we investigated amyloid metabolism in patients with Lyme neuroborreliosis (LNB). Methods: The first part of the study was a cross-sectional cohort study in 61 patients with acute facial palsy (19 with LNB and 42 with idiopathic facial paresis, Bell's palsy) and 22 healthy controls. CSF was analysed for the beta-amyloid peptides A beta 38, A beta 40 and A beta 42, and the amyloid precursor protein (APP) isoforms alpha-sAPP and beta-sAPP. CSF total-tau (T-tau), phosphorylated tau (P-tau) and neurofilament protein (NFL) were measured to monitor neural cell damage. The second part of the study was a prospective cohort-study in 26 LNB patients undergoing consecutive lumbar punctures before and after antibiotic treatment to study time-dependent dynamics of the biomarkers. Results: In the cross-sectional study, LNB patients had lower levels of CSF alpha-sAPP, beta-sAPP and P-tau, and higher levels of CSF NFL than healthy controls and patients with Bell's palsy. In the prospective study, LNB patients had low levels of CSF alpha-sAPP, beta-sAPP and P-tau at baseline, which all increased towards normal at follow-up. Conclusions: Amyloid metabolism is altered in LNB. CSF levels of alpha-sAPP, beta-sAPP and P-tau are decreased in acute infection and increase after treatment. In combination with earlier findings in multiple sclerosis, cerebral SLE and HIV with cerebral engagement, this points to an influence of neuroinflammation on amyloid metabolism. (Less)
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author
organization
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Contribution to journal
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published
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in
BMC Neurology
volume
10
publisher
BioMed Central
external identifiers
  • wos:000279941400001
  • scopus:77954657208
ISSN
1471-2377
DOI
10.1186/1471-2377-10-51
language
English
LU publication?
yes
id
122c9eb3-67ed-41d0-a2bc-35c0b6b72f8c (old id 1657598)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20569437?dopt=AbstractPlus&holding=f1000,f1000m,isrctn
date added to LUP
2010-08-24 13:27:04
date last changed
2018-07-15 03:49:57
@article{122c9eb3-67ed-41d0-a2bc-35c0b6b72f8c,
  abstract     = {Background: The metabolism of amyloid precursor protein (APP) and beta-amyloid (A beta) is widely studied in Alzheimer's disease, where A beta deposition and plaque development are essential components of the pathogenesis. However, the physiological role of amyloid in the adult nervous system remains largely unknown. We have previously found altered cerebral amyloid metabolism in other neuroinflammatory conditions. To further elucidate this, we investigated amyloid metabolism in patients with Lyme neuroborreliosis (LNB). Methods: The first part of the study was a cross-sectional cohort study in 61 patients with acute facial palsy (19 with LNB and 42 with idiopathic facial paresis, Bell's palsy) and 22 healthy controls. CSF was analysed for the beta-amyloid peptides A beta 38, A beta 40 and A beta 42, and the amyloid precursor protein (APP) isoforms alpha-sAPP and beta-sAPP. CSF total-tau (T-tau), phosphorylated tau (P-tau) and neurofilament protein (NFL) were measured to monitor neural cell damage. The second part of the study was a prospective cohort-study in 26 LNB patients undergoing consecutive lumbar punctures before and after antibiotic treatment to study time-dependent dynamics of the biomarkers. Results: In the cross-sectional study, LNB patients had lower levels of CSF alpha-sAPP, beta-sAPP and P-tau, and higher levels of CSF NFL than healthy controls and patients with Bell's palsy. In the prospective study, LNB patients had low levels of CSF alpha-sAPP, beta-sAPP and P-tau at baseline, which all increased towards normal at follow-up. Conclusions: Amyloid metabolism is altered in LNB. CSF levels of alpha-sAPP, beta-sAPP and P-tau are decreased in acute infection and increase after treatment. In combination with earlier findings in multiple sclerosis, cerebral SLE and HIV with cerebral engagement, this points to an influence of neuroinflammation on amyloid metabolism.},
  author       = {Mattsson, Niklas and Bremell, Daniel and Anckarsater, Rolf and Blennow, Kaj and Anckarsäter, Henrik and Zetterberg, Henrik and Hagberg, Lars},
  issn         = {1471-2377},
  language     = {eng},
  publisher    = {BioMed Central},
  series       = {BMC Neurology},
  title        = {Neuroinflammation in Lyme neuroborreliosis affects amyloid metabolism},
  url          = {http://dx.doi.org/10.1186/1471-2377-10-51},
  volume       = {10},
  year         = {2010},
}