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Article type: Research Article
Authors: Renard, Dimitria; * | Wacongne, Annea | Ayrignac, Xavierb; c | Charif, Mahmoudb | Fourcade, Genevieved | Azakri, Souhaylaa | Le Floch, Annea | Bouly, Stephanea | Marelli, Ceciliab | Arquizan, Carolineb | Hirtz, Christophef | Gabelle, Audreye; f | Thouvenot, Ericg | Lehmann, Sylvainf
Affiliations: [a] Department of Neurology, CHU Nîmes, Hôpital Caremeau, Rue du Pr Debré, Nîmes Cedex, France | [b] Department of Neurology, CHU Montpellier, Hôpital Gui de Chauliac, Montpellier, France | [c] The Neuroscience Institute of Montpellier (INM), Inserm UMR1051, CHU Montpellier, Hôpital Saint-Eloi, Montpellier, France | [d] Department of Neurology, CH Narbonne, Narbonne, France | [e] Centre Mémoire de Resources et de Recherche Montpellier, CHU Montpellier, Hôpital Gui de Chauliac –Université de Montpellier, Montpellier Cedex, France | [f] Laboratoire de Biochimie-Protéomique Clinique –IRMB –CCBHM - Inserm U11183, CHU Montpellier, Hôpital St-Eloi - Université Montpellier, Montpellier Cedex, France | [g] Department of Neurology, CHU Nîmes, Hôpital Caremeau –Université de Montpellier, Nîmes Cedex, France
Correspondence: [*] Correspondence to: Dimitri Renard, MD, Department of Neurology, CHU Nîmes, Hôpital Caremeau, 4, Rue du Pr Debré, 30029 Nîmes Cedex 4, France. Tel.: +33466683261; Fax: +33466684016; E-mail: [email protected].
Abstract: Background:Decreased cerebrospinal fluid (CSF) amyloid-β 1-40 (Aβ40) and amyloid-β 1-42 (Aβ42) and increased total and phosphorylated tau (t-tau, p-tau) concentrations have been described in cerebral amyloid angiopathy (CAA). Objective:Our aim was to analyze these biomarkers in patients with CAA-related inflammation (CAA-I). Methods:We prospectively recruited nine patients with acute phase CAA-I fulfilling Chung criteria. CSF was analyzed for t-tau, p-tau, Aβ42, and Aβ40. Data were compared to controls (n = 14), patients with Alzheimer’s disease (AD, n = 42), CAA (n = 10), and primary angiitis of the central nervous system (PACNS, n = 3). Results:For the CAA-I group, statistically significant differences were: lower Aβ42 (p = 0.00053) compared to the control group; lower t-tau (p = 0.018), p-tau (p < 0.001), and Aβ40 (p < 0.001) compared to AD; lower Aβ42 (p = 0.027) compared to CAA; lower Aβ42 (p = 0.012) compared to PACNS. Nearly significantly lower Aβ40 (p = 0.051) and higher t-tau (p = 0.051) were seen in CAA-I compared to controls. Conclusion:CSF biomarkers profile similar to that of CAA was observed in CAA-I (with even lower levels of Aβ42 compared to CAA). Based on our findings, high p-tau seems more specific for AD, whereas low Aβ42 differentiates CAA-I from CAA, PACNS, and controls, and low Aβ40 differentiates CAA-I from AD.
Keywords: Alzheimer’s disease, amyloid-β, cerebral amyloid angiopathy, cerebrospinal fluid, inflammation, tau
DOI: 10.3233/JAD-150621
Journal: Journal of Alzheimer's Disease, vol. 50, no. 3, pp. 759-764, 2016
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