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Article type: Short Communication
Authors: Glodzik, Lidiaa; * | De Santi, Susana | Rich, Kenneth E.a | Brys, Miroslawa | Pirraglia, Elizabetha | Mistur, Rachela | Switalski, Remigiuszb | Mosconi, Lisaa | Sadowski, Martinc | Zetterberg, Henrikd | Blennow, Kajd | de Leon, Mony J.a; e
Affiliations: [a] Center for Brain Health, Department of Psychiatry, New York University School of Medicine, New York, NY, USA | [b] Department of Family Medicine, East Tennessee State University, Johnson City, TN, USA | [c] Department of Neurology, New York University School of Medicine, New York, NY, USA | [d] University of Goteborg, Sahlgrenska University Hospital, Goteborg, Sweden | [e] Nathan Kline Institute, Orangeburg, NY, USA
Correspondence: [*] Address for correspondence: Lidia Glodzik, Center for Brain Health, New York University School of Medicine, 145 East 32nd Street, 5th Floor, New York, NY NY 10016, USA. Tel.: +1 212 263 5698; Fax: +1 212 263 3270; E-mail: Lidia.Glodzik-Sobanska@nyumc.org.
Abstract: Previous studies showed that memantine inhibits tau hyperphosphorylation in vitro. In this study, phosphorylated tau (P-tau) and total tau (T-tau) were measured before and after 6 month treatment with memantine in 12 subjects ranging from normal cognition with subjective memory complaints, through mild cognitive impairment to mild Alzheimer's disease. Thirteen non-treated individuals served as controls. Treatment was associated with a reduction of P-tau in subjects with normal cognition. No treatment effects were seen among impaired individuals, suggesting that longer treatment time may be necessary to achieve biomarker effect in this group.
Keywords: Alzheimer's disease, biomarkers, cerebrospinal fluid, memantine, phosphorylated tau, total tau
DOI: 10.3233/JAD-2009-1183
Journal: Journal of Alzheimer's Disease, vol. 18, no. 3, pp. 509-513, 2009
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