title: Amyloid-related biomarkers and axonal damage proteins in parkinsonian syndromes.
abstract: BACKGROUND
  Clinical differentiation between parkinsonian syndromes (PS) remains a challenge despite well-established clinical diagnostic criteria. Specific diagnostic biomarkers have yet to be identified, though in recent years, studies have been published on the aid of certain brain related proteins (BRP) in the diagnosing of PS. We investigated the levels of the light subunit of neurofilament triplet protein (NF-L), total tau and phosphorylated tau, amyloid-β(1-42), and the soluble α- and β-cleaved fragments of amyloid precursor proteins in a cohort of patients with various PS.
  
  
  METHODS
  Seventy-one patients with different PS and cerebellar disorders were included consecutively over 21 months. CSF was collected at inclusion. Clinical follow-up was performed after 16 months (median; range: 9-30). Statistical comparison was performed after follow-up on 53 patients in four subgroups of PS: multiple system atrophy (MSA)(n = 10), progressive supranuclear palsy (PSP)(n = 10), dementia with Lewy bodies (DLB)(n = 11), and Parkinson's disease (PD)(n = 22), using the non-parametric Kruskal-Wallis test.
  
  
  RESULTS
  A statistically significant difference was found for NF-L (p < 0.0001, lowest values for PD), Aβ(1-42,) (p = 0.002, lowest values for DLB), and sAPPα and sAPPβ (p = 0.03 and 0.02, lower values observed for DLB and MSA).
  
  
  CONCLUSIONS
  We demonstrate a potential role for sAPPα and sAPPβ in distinguishing between PS, a finding that needs to be confirmed in future studies of larger cohorts. There is a tendency towards low levels of Aβ(1-42) in DLB patients in our cohort. Further, our results support findings from previous studies, which indicate an ability to separate atypical PS from PD based on levels of NF-L.
authors.affiliation: Department of Neurology, Bispebjerg Hospital, Copenhagen University Hospital, Copenhagen, Denmark. sarabw@sund.ku.dk
authors.forename: Sara
authors.initials: S
authors.lastname: Bech
authors.forename: Lena E
authors.initials: LE
authors.lastname: Hjermind
authors.forename: Lisette
authors.initials: L
authors.lastname: Salvesen
authors.forename: Jørgen E
authors.initials: JE
authors.lastname: Nielsen
authors.forename: Niels H H
authors.initials: NH
authors.lastname: Heegaard
authors.forename: Henrik L
authors.initials: HL
authors.lastname: Jørgensen
authors.forename: Lars
authors.initials: L
authors.lastname: Rosengren
authors.forename: Kaj
authors.initials: K
authors.lastname: Blennow
authors.forename: Henrik
authors.initials: H
authors.lastname: Zetterberg
authors.forename: Kristian
authors.initials: K
authors.lastname: Winge
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid*; D016564:Amyloid beta-Protein Precursor / Q000134:cerebrospinal fluid*; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers / Q000134:cerebrospinal fluid; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D016900:Neurofilament Proteins / Q000134:cerebrospinal fluid*; D020734:Parkinsonian Disorders / Q000134:cerebrospinal fluid* / Q000175:diagnosis; D010446:Peptide Fragments / Q000134:cerebrospinal fluid*; D016875:tau Proteins / Q000134:cerebrospinal fluid*
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D015415:Biomarkers; D016900:Neurofilament Proteins; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D016875:tau Proteins