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Article type: Short Communication
Authors: Courtemanche, Hélènea | Bigot, Edithb | Pichelin, Matthieuc; d; e | Guyomarch, Béatriced | Boutoleau-Bretonnière, Clairea | Le May, Cédrice | Derkinderen, Pascala | Cariou, Bertrandc; d; e; *
Affiliations: [a] Department of Neurology, CHU de Nantes, Nantes, France | [b] Department of Biochemistry, CHU de Nantes, Nantes, France | [c] L’institut du thorax, Department of Endocrinology, CHU Nantes, Nantes, France | [d] L’institut du thorax, CIC Endocrino-Nutrtition, CHU Nantes, Nantes, France | [e] L’institut du thorax, INSERM, CNRS, UNIV NANTES, Nantes, France
Correspondence: [*] Correspondence to: Bertrand Cariou, Clinique d’Endocrinologie, Hôpital Guillaume and René Laennec, Boulevard Jacques Monod, Saint-Herblain, 44093 Nantes Cedex 1, France. Tel.: +00 33 2 53 48 27 07; Fax: +00 33 2 53 48 27 08; E-mail: [email protected].
Abstract: The role of PCSK9 in Alzheimer’s disease (AD) is controversial. We compared cerebrospinal fluid (CSF) PCSK9 concentrations in 36 AD and 31 non-AD patients. CSF PCSK9 levels did not differ between AD and non-AD groups (2.80 versus 2.62 ng/mL). However, PCSK9 CSF levels were increased in AD and non-AD patients with other neurodegenerative process (non-AD ND, n = 20) compared to patients without neurodegenerative disorders (non-ND, n = 11): 2.80 versus 2.30 (p < 0.005) and 2.83 versus 2.30 ng/mL (p = NS), respectively. CSF PCSK9 were positively correlated with AD biomarkers (Aβ1-42, T-tau, and P-tau). PCSK9 concentrations in CSF are increased in neurodegenerative disorders rather than specifically in AD.
Keywords: Aβ1-42, cerebrospinal fluid, frontotemporal lobar degeneration, LDL-cholesterol, P-tau, PCSK9, T-tau
DOI: 10.3233/JAD-170993
Journal: Journal of Alzheimer's Disease, vol. 62, no. 4, pp. 1519-1525, 2018
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