• Dimitri Renard, Anne Wacongne, Xavier Ayrignac, Mahmoud Charif, Genevieve Fourcade, Souhayla Azakri, Anne Le Floch, Stephane Bouly, Cecilia Marelli, Caroline Arquizan, Christophe Hirtz, Audrey Gabelle, Eric Thouvenot, and Sylvain Lehmann.
• Department of Neurology, CHU Nîmes, Hôpital Caremeau, Rue du Pr Debré, Nîmes Cedex, France.
• J. Alzheimers Dis. 2016 Jan 1; 50 (3): 759-764.

BackgroundDecreased 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).ObjectiveOur aim was to analyze these biomarkers in patients with CAA-related inflammation (CAA-I).MethodsWe 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).ResultsFor 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.ConclusionCSF 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.

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