title: CSF biomarkers in posterior cortical atrophy.
abstract: OBJECTIVE
  To describe CSF biomarker profiles in posterior cortical atrophy (PCA), which induces high-order visual deficits often associated with Alzheimer disease (AD) pathology, and relate these findings to clinical and neuropsychological assessment.
  
  
  METHODS
  This prospective observational study included 22 patients with PCA who underwent CSF biomarker analysis of total tau (t-tau), phosphorylated tau on amino acid 181 (p-tau181), and amyloid β (Aβ(42)). At group level, the CSF profiles of patients with PCA were compared to those of patients with typical AD and patients with other dementia (OD). Individually, the clinical presentation of patients with PCA was correlated to their CSF profile to assess the predictability of clinical features for diagnosis of underlying AD pathology.
  
  
  RESULTS
  At group level, the PCA biomarker profile was not different from that of the AD group, but very different from that of the OD group (p < 0.001). More than 90% of patients with PCA had CSF profiles consistent with AD. All patients with PCA with either isolated higher-order visual deficit (n = 8) or visual deficit associated with memory impairment (n = 11) had CSF profiles consistent with AD. Only one of the 3 patients with PCA with asymmetric motor signs fulfilled biological CSF criteria for AD.
  
  
  CONCLUSIONS
  PCA syndrome is usually associated with CSF biomarkers suggestive of AD, as shown by previous neuropathologic studies. This does not apply in case of motor signs suggesting associated corticobasal syndrome. CSF biomarkers help to discriminate AD from non-AD processes associated with this condition.
authors.affiliation: Department of Biochemistry, Hôpital Neurologique, Hospices Civils de Lyon, Lyon, France.
authors.forename: J
authors.initials: J
authors.lastname: Seguin
authors.forename: M
authors.initials: M
authors.lastname: Formaglio
authors.forename: A
authors.initials: A
authors.lastname: Perret-Liaudet
authors.forename: I
authors.initials: I
authors.lastname: Quadrio
authors.forename: Y
authors.initials: Y
authors.lastname: Tholance
authors.forename: O
authors.initials: O
authors.lastname: Rouaud
authors.forename: C
authors.initials: C
authors.lastname: Thomas-Anterion
authors.forename: B
authors.initials: B
authors.lastname: Croisile
authors.forename: H
authors.initials: H
authors.lastname: Mollion
authors.forename: O
authors.initials: O
authors.lastname: Moreaud
authors.forename: M
authors.initials: M
authors.lastname: Salzmann
authors.forename: A
authors.initials: A
authors.lastname: Dorey
authors.forename: M
authors.initials: M
authors.lastname: Bataillard
authors.forename: M-H
authors.initials: MH
authors.lastname: Coste
authors.forename: A
authors.initials: A
authors.lastname: Vighetto
authors.forename: P
authors.initials: P
authors.lastname: Krolak-Salmon
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid; D001284:Atrophy / Q000134:cerebrospinal fluid* / Q000175:diagnosis / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers / Q000134:cerebrospinal fluid; D002540:Cerebral Cortex / Q000473:pathology*; D003704:Dementia / Q000134:cerebrospinal fluid / Q000175:diagnosis / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D011446:Prospective Studies; D013577:Syndrome; D014786:Vision Disorders / Q000134:cerebrospinal fluid / Q000473:pathology / Q000503:physiopathology; D016875:tau Proteins / Q000134:cerebrospinal fluid
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D016875:tau Proteins