Searching for just a few words should be enough to get started. If you need to make more complex queries, use the tips below to guide you.
Article type: Research Article
Authors: Santangelo, Robertoa; * | Cecchetti, Giordanoa | Bernasconi, Maria Paolaa | Cardamone, Rosalindaa | Barbieri, Alessandraa | Pinto, Patriziab | Passerini, Gabriellac | Scomazzoni, Francescod | Comi, Giancarloa | Magnani, Giuseppea
Affiliations: [a] Department of Neurology, INSPE, Vita-Salute University and IRCCS-San Raffaele Hospital, Milan, Italy | [b] Department of Neurology, Papa Giovanni XXIII Hospital, Bergamo, Italy | [c] Laboraf, IRCCS-San Raffaele Hospital, Milan, Italy | [d] Department of Neuroradiology, Vita-Salute University and IRCCS-San Raffaele Hospital, Milan, Italy
Correspondence: [*] Correspondence to: Roberto Santangelo, Department of Neurology, San Raffaele Hospital, via Olgettina 48, 20132 Milan, Italy. E-mail: santangelo.roberto@hsr.it.
Abstract: Co-existence of Alzheimer’s disease (AD) in normal pressure hydrocephalus (NPH) is a frequent finding, thus a common pathophysiological basis between AD and NPH has been postulated. We measured CSF amyloid-β 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) concentrations in a sample of 294 patients with different types of dementia and 32 subjects without dementia. We then compared scores on neuropsychological tests of NPH patients with pathological and normal CSF Aβ42 values. Aβ42 levels were significantly lower in NPH than in control patients, with no significant differences between AD and NPH. On the contrary, t-tau and p-tau levels were significantly lower in NPH than in AD, with no differences between NPH and controls. NPH patients with pathological Aβ42 levels did not perform worse than NPH patients with normal Aβ42 levels in any cognitive domains. Our data seem to support the hypothesis of amyloid accumulation in brains of NPH patients. Nevertheless, amyloid does not seem to play a pathogenetic role in the development of cognitive deficits in NPH.
Keywords: Amyloid-β 42, cerebral amyloid burden, glymphatic system, normal pressure hydrocephalus, phosphorylated tau, tau protein
DOI: 10.3233/JAD-170186
Journal: Journal of Alzheimer's Disease, vol. 60, no. 1, pp. 183-200, 2017
IOS Press, Inc.
6751 Tepper Drive
Clifton, VA 20124
USA
Tel: +1 703 830 6300
Fax: +1 703 830 2300
sales@iospress.com
For editorial issues, like the status of your submitted paper or proposals, write to editorial@iospress.nl
IOS Press
Nieuwe Hemweg 6B
1013 BG Amsterdam
The Netherlands
Tel: +31 20 688 3355
Fax: +31 20 687 0091
info@iospress.nl
For editorial issues, permissions, book requests, submissions and proceedings, contact the Amsterdam office info@iospress.nl
Inspirees International (China Office)
Ciyunsi Beili 207(CapitaLand), Bld 1, 7-901
100025, Beijing
China
Free service line: 400 661 8717
Fax: +86 10 8446 7947
china@iospress.cn
For editorial issues, like the status of your submitted paper or proposals, write to editorial@iospress.nl
如果您在出版方面需要帮助或有任何建, 件至: editorial@iospress.nl