| Literature DB >> 26446019 |
Minsook Ye1, Hwan-Suck Chung2, Yong Ho An3, Su-Jin Lim1, Won Choi1, A Ram Yu4, Jin Su Kim4, Manho Kang1, Seunghun Cho5, Insop Shim2, Hyunsu Bae6.
Abstract
Alzheimer's disease (AD) is a severe neurodegenerative disease for which there is currently no effective treatment. This study investigated whether treatment with the herbal formula PM012 would improve the cognitive function and the pathological features of AD in 3xTg-AD mice. The cognitive function of 3xTg-AD mice was assessed using the Morris water maze test and positron-emission tomography (PET) with 18 F-2 fluoro-2-deoxy-D-glucose ([F-18] FDG) neuroimaging. The levels of the amyloid beta (Aβ) deposits in the hippocampus were evaluated by immunohistochemistry. Neurogenesis was assessed by quantitative labeling with the DNA marker bromodeoxyuridine (BrdU) and the newborn neuron marker doublecortin (DCX). PM012 treatment significantly ameliorated memory deficit in AD mice, as shown by shortened escape latencies and increased time spent in the target zone during probe tests. In addition, PM012 significantly decreased Aβ deposits, up-regulated the expression of brain-derived neurotrophic factor (BDNF), increased neurogenesis, and improved brain glucose metabolism in the 3xTg-AD mice. These results suggest that PM012 could be a promising treatment for AD.Entities:
Keywords: 3xTg AD; Alzheimer’s disease; Beta-amyloid; Neurogenesis; PET; PM012
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Year: 2015 PMID： 26446019 DOI： 10.1007/s12035-015-9458-x
Source DB: PubMed Journal: Mol Neurobiol ISSN： 0893-7648 Impact factor: 5.590