| Literature DB >> 27079710 |
Masaaki Waragai1,2, Anthony Adame3, Ivy Trinh3, Kazunari Sekiyama2, Yoshiki Takamatsu2, Kaori Une4, Eliezer Masliah3, Makoto Hashimoto2.
Abstract
Adiponectin (APN) is protective in animal models of neurodegenerative diseases, but the role of APN in human brain has not been established. Using an enzyme-linked immunosorbent assay, we found that APN was significantly decreased in cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), compared to those in patients with mild cognitive impairment (MCI) and in normal controls (NC), despite elevation of APN in serum of patients with MCI and AD compared to that in NC. The discrepancy of CSF APN from serum APN in AD may suggest some critical actions of APN in the pathogenesis of AD. Indeed, it was histologically observed that APN was co-localized with tau in neurofibrillary tangles and immunoblot analysis showed that the functional trimers of APN were significantly decreased in AD compared to those in NC. Collectively, a loss of function of APN may be involved in the pathogenesis of AD.Entities:
Keywords: Adiponectin; Alzheimer’s disease; cerebrospinal fluid; neurofibrillary tangles; sequestration; serum; tau
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Year: 2016 PMID: 27079710 DOI: 10.3233/JAD-151116
Source DB: PubMed Journal: J Alzheimers Dis ISSN: 1387-2877 Impact factor: 4.472