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J Alzheimers Dis. 2016;50(3):759-764. doi: 10.3233/JAD-150621.

Cerebrospinal Fluid Alzheimer's Disease Biomarkers in Cerebral Amyloid Angiopathy-Related Inflammation.

Author information

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.

KEYWORDS:

Alzheimer’s disease; amyloid-β; cerebral amyloid angiopathy; cerebrospinal fluid; inflammation; tau

PMID:
26757185
PMCID:
PMC6294577
DOI:
10.3233/JAD-150621
[Indexed for MEDLINE]
Free PMC Article

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