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Mol Neurobiol. 2016 Oct;53(8):5401-12. doi: 10.1007/s12035-015-9458-x. Epub 2015 Oct 7.

Standardized Herbal Formula PM012 Decreases Cognitive Impairment and Promotes Neurogenesis in the 3xTg AD Mouse Model of Alzheimer's Disease.

Author information

1
Department of Physiology, College of Korean Medicine, Kyung Hee University, #1, Hoegi-dong, Dongdaemoon-ku, Seoul, 130-701, Republic of Korea.
2
Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), 70, Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea.
3
Acupuncture and Meridian Science Research Center, College of Korean Medical Science Graduate School, Kyung Hee University, #1 Hoegi-dong, Dongdaemoon-ku, Seoul, 130-701, Republic of Korea.
4
Molecular Imaging Research Center, Korea Institute of Radiological & Medical Sciences University of Science & Technology, #215-4 Gongneug-dong, Nowon-ku, Seoul, 139-241, Republic of Korea.
5
Hospital of Korean Medicine Kyung Hee University Medical Center, #1 Hoegi-dong, Dongdaemoon-ku, Seoul, 130-701, Republic of Korea.
6
Department of Physiology, College of Korean Medicine, Kyung Hee University, #1, Hoegi-dong, Dongdaemoon-ku, Seoul, 130-701, Republic of Korea. hbae@khu.ac.kr.

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.

KEYWORDS:

3xTg AD; Alzheimer’s disease; Beta-amyloid; Neurogenesis; PET; PM012

PMID:
26446019
DOI:
10.1007/s12035-015-9458-x
[Indexed for MEDLINE]

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