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Article type: Short Communication
Authors: Verwey, Nicolaas A.a; * | Teunissen, Charlotte E.b | Hoozemans, Jeroen J.M.c | Rozemuller, Annemieke J.M.c | Scheltens, Philipd | Pijnenburg, Yolande A.L.d
Affiliations: [a] Department of Neurology, Medisch Centrum Leeuwarden, The Netherlands | [b] Departments of Clinical Chemistry, Amsterdam University Medical Center location VUmc, Alzheimer Center, Amsterdam, The Netherlands | [c] Departments of Pathology, Amsterdam University Medical Center location VUmc, Alzheimer Center, Amsterdam, The Netherlands | [d] Departments of Neurology, Amsterdam University Medical Center location VUmc, Alzheimer Center, Amsterdam, The Netherlands
Correspondence: [*] Correspondence to: N.A. Verwey, MD, PhD, Department of Neurology, Henri Dunantweg 2, 8934 AD, Leeuwarden, the Netherlands. Tel.: +0031 0 58 2863929; E-mail: [email protected].
Abstract: To investigate amyloid-β (Aβ) in frontotemporal dementia (FTD), cerebrospinal fluid (CSF) Aβ38, Aβ40, and Aβ42 in frontotemporal lobar degeneration (FTLD; N = 18 genetically and/or pathologically confirmed and N = 8 FTD with concomitant amyotrophic lateral sclerosis) were compared with Alzheimer’s disease (AD; pathological or Pittsburgh-compound-B Positron-emission-tomography (PIB-PET) positive; N = 25) and controls (N = 24). For all the Aβ subtypes, group difference was seen and post-hoc analysis revealed lower levels in FTLD compared to controls (p≤0.05). Aβ42/40 ratio showed no difference between FTLD and controls; however, a difference was seen between AD versus FTLD (p < 0.01). This is an intriguing finding, suggesting a possible role of Aβ in FTLD pathogenesis.
Keywords: Alzheimer’s disease, amyloid, frontotemporal dementia, frontotemporal lobar degeneration
DOI: 10.3233/JAD-190344
Journal: Journal of Alzheimer's Disease, vol. 71, no. 1, pp. 15-20, 2019
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