Dimitri Renard1, Anne Wacongne1, Xavier Ayrignac2,3, Mahmoud Charif2, Genevieve Fourcade4, Souhayla Azakri1, Anne Le Floch1, Stephane Bouly1, Cecilia Marelli2, Caroline Arquizan2, Christophe Hirtz5, Audrey Gabelle6,5, Eric Thouvenot7, Sylvain Lehmann5. 1. Department of Neurology, CHU Nîmes, Hôpital Caremeau, Rue du Pr Debré, Nîmes Cedex, France. 2. Department of Neurology, CHU Montpellier, Hôpital Gui de Chauliac, Montpellier, France. 3. The Neuroscience Institute of Montpellier (INM), Inserm UMR1051, CHU Montpellier, Hôpital Saint-Eloi, Montpellier, France. 4. Department of Neurology, CH Narbonne, Narbonne, France. 5. Laboratoire de Biochimie-Protéomique Clinique -IRMB -CCBHM - Inserm U11183, CHU Montpellier, Hôpital St-Eloi - Université Montpellier, Montpellier Cedex, France. 6. Centre Mémoire de Resources et de Recherche Montpellier, CHU Montpellier, Hôpital Gui de Chauliac -Université de Montpellier, Montpellier Cedex, France. 7. Department of Neurology, CHU Nîmes, Hôpital Caremeau -Université de Montpellier, Nîmes Cedex, France.
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.
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.
Authors: L Grangeon; G Quesney; X Ayrignac; D Wallon; M Verdalle-Cazes; S Coulette; D Renard; A Wacongne; T Allou; N Olivier; Y Boukriche; G Blanchet-Fourcade; P Labauge; C Arquizan; S Canaple; O Godefroy; O Martinaud; P Verdure; M Quillard-Muraine; J Pariente; E Magnin; G Nicolas; C Charbonnier; D Maltête; M Formaglio; N Raposo Journal: J Neurol Date: 2022-06-26 Impact factor: 6.682
Authors: Gargi Banerjee; Roxana Carare; Charlotte Cordonnier; Steven M Greenberg; Julie A Schneider; Eric E Smith; Mark van Buchem; Jeroen van der Grond; Marcel M Verbeek; David J Werring Journal: J Neurol Neurosurg Psychiatry Date: 2017-08-26 Impact factor: 10.154
Authors: Linda J C van Waalwijk van Doorn; Luka Kulic; Marleen J A Koel-Simmelink; H Bea Kuiperij; Alexandra A M Versleijen; Hanne Struyfs; Harry A M Twaalfhoven; Anthony Fourier; Sebastiaan Engelborghs; Armand Perret-Liaudet; Sylvain Lehmann; Marcel M Verbeek; Eugeen J M Vanmechelen; Charlotte E Teunissen Journal: Front Neurol Date: 2017-07-03 Impact factor: 4.003
Authors: Jeremy A Tanner; Megan B Richie; Cathryn R Cadwell; Amity Eliaz; Shannen Kim; Zeeshan Haq; Nailyn Rasool; Maulik P Shah; Elan L Guterman Journal: BMC Neurol Date: 2022-03-24 Impact factor: 2.474