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Metformin and neural stem cells

Ming-Chang Chiang, Yi-Chuan Cheng, Shiang-Jiuun Chen, Chia-Hui Yen, Rong-Nan Huang
Alzheimer's disease (AD) is the general consequence of dementia and is diagnostic neuropathology by the cumulation of amyloid-beta (Aβ) protein aggregates, which are thought to promote mitochondrial dysfunction processes leading to neurodegeneration. AMP-activated protein kinase (AMPK), a critical regulator of energy homeostasis and a major player in lipid and glucose metabolism, is potentially implied in the mitochondrial deficiency of AD. Metformin, one of the widespread used anti- metabolic disease drugs, use its actions in part by stimulation of AMPK...
October 1, 2016: Experimental Cell Research
Rouknuddin Qasim Ali, Evelina Blomberg, Anna Falk, Lars Ährlund-Richter, Mats Ulfendahl
Hearing impairment most often involves loss of sensory hair cells and auditory neurons. As this loss is permanent in humans, a cell therapy approach has been suggested to replace damaged cells. It is thus of interest to generate lineage restricted progenitor cells appropriate for cell based therapies. Human long-term self-renewing neuroepithelial stem (lt-NES) cell lines exhibit in vitro a developmental potency to differentiate into CNS neural lineages, and importantly lack this potency in vivo, i.e do not form teratomas...
2016: American Journal of Stem Cells
Michael Fatt, Karolynn Hsu, Ling He, Fredric Wondisford, Freda D Miller, David R Kaplan, Jing Wang
The recruitment of endogenous adult neural stem cells for brain repair is a promising regenerative therapeutic strategy. This strategy involves stimulation of multiple stages of adult neural stem cell development, including proliferation, self-renewal, and differentiation. Currently, there is a lack of a single therapeutic approach that can act on these multiple stages of adult neural stem cell development to enhance neural regeneration. Here we show that metformin, an FDA-approved diabetes drug, promotes proliferation, self-renewal, and differentiation of adult neural precursors (NPCs)...
December 8, 2015: Stem Cell Reports
Poulomi Banerjee, Sunit Dutta, Rajarshi Pal
Neural crest cells (NCC) are a population of epithelial cells that arise from the dorsal tube and undergo epithelial-mesenchymal transition (EMT) eventually generating tissues from peripheral nervous system, melanocytes, craniofacial cartilage, and bone. The antidiabetic drug metformin reportedly inhibits EMT in physiological conditions like cancer and fibrosis. We hypothesize that perturbation of EMT may also contribute to developmental disabilities associated with neural crest (NC) development. To understand the molecular network underlying metformin action during NC formation, we first differentiated murine embryonic stem (ES) cells into NCC and characterized them by demonstrating spatiotemporal regulation of key markers...
February 2016: Stem Cells
Parvati Dadwal, Neemat Mahmud, Laleh Sinai, Ashkan Azimi, Michael Fatt, Fredric E Wondisford, Freda D Miller, Cindi M Morshead
The development of cell replacement strategies to repair the injured brain has gained considerable attention, with a particular interest in mobilizing endogenous neural stem and progenitor cells (known as neural precursor cells [NPCs]) to promote brain repair. Recent work demonstrated metformin, a drug used to manage type II diabetes, promotes neurogenesis. We sought to determine its role in neural repair following brain injury. We find that metformin administration activates endogenous NPCs, expanding the size of the NPC pool and promoting NPC migration and differentiation in the injured neonatal brain in a hypoxia-ischemia (H/I) injury model...
August 11, 2015: Stem Cell Reports
Ming-Min Chung, Yen-Lin Chen, Dee Pei, Yi-Chuan Cheng, Binggui Sun, Christopher J Nicol, Chia-Hui Yen, Han-Min Chen, Yao-Jen Liang, Ming-Chang Chiang
Diabetic neuronal damage results from hyperglycemia followed by increased formation of advanced glycosylation end products (AGEs), which leads to neurodegeneration, although the molecular mechanisms are still not well understood. Metformin, one of the most widely used anti-diabetic drugs, exerts its effects in part by activation of AMP-activated protein kinase (AMPK). AMPK is a critical evolutionarily conserved enzyme expressed in the liver, skeletal muscle and brain, and promotes cellular energy homeostasis and biogenesis by regulating several metabolic processes...
May 2015: Biochimica et Biophysica Acta
Hyung-Yul Lee, Dan Wei, Mary R Loeken
BACKGROUND: Adenosine monophosphate-activated protein kinase (AMPK) is stimulated in embryos during diabetic pregnancy by maternal hyperglycaemia-induced embryo oxidative stress. Stimulation of AMPK disrupts embryo gene expression and causes neural tube defects. Metformin, which may be taken during early pregnancy, has been reported to stimulate AMPK activity. Thus, the benefits of improved glycaemic control could be offset by stimulated embryo AMPK activity. Here, we investigated whether metformin can stimulate AMPK activity in mouse embryos and can adversely affect embryo gene expression and neural tube defects...
January 2014: Diabetes/metabolism Research and Reviews
Yael Kusne, Emily L Goldberg, Sara S Parker, Sophie M Hapak, Irina Y Maskaykina, Wade M Chew, Kirsten H Limesand, Heddwen L Brooks, Theodore J Price, Nader Sanai, Janko Nikolich-Zugich, Sourav Ghosh
The chronic and systemic administration of rapamycin extends life span in mammals. Rapamycin is a pharmacological inhibitor of mTOR. Metformin also inhibits mTOR signaling but by activating the upstream kinase AMPK. Here we report the effects of chronic and systemic administration of the two mTOR inhibitors, rapamycin and metformin, on adult neural stem cells of the subventricular region and the dendate gyrus of the mouse hippocampus. While rapamycin decreased the number of neural progenitors, metformin-mediated inhibition of mTOR had no such effect...
February 2014: Age (2005-)
Jing Wang, Denis Gallagher, Loren M DeVito, Gonzalo I Cancino, David Tsui, Ling He, Gordon M Keller, Paul W Frankland, David R Kaplan, Freda D Miller
Although endogenous recruitment of adult neural stem cells has been proposed as a therapeutic strategy, clinical approaches for achieving this are lacking. Here, we show that metformin, a widely used drug, promotes neurogenesis and enhances spatial memory formation. Specifically, we show that an atypical PKC-CBP pathway is essential for the normal genesis of neurons from neural precursors and that metformin activates this pathway to promote rodent and human neurogenesis in culture. Metformin also enhances neurogenesis in the adult mouse brain in a CBP-dependent fashion, and in so doing enhances spatial reversal learning in the water maze...
July 6, 2012: Cell Stem Cell
Matthew B Potts, Daniel A Lim
Identifying well-tolerated, oral medications that enhance adult neurogenesis is of great clinical interest. In this issue of Cell Stem Cell, Wang et al. (2012) demonstrate that the diabetes medication metformin enhances spatial learning in mice by activating the atypical PKC/CBP pathway in adult neural stem cells.
July 6, 2012: Cell Stem Cell
Melanie Swan
The focus of the 2011 American Aging Association meeting was emerging concepts in the mechanisms of aging. Many of the usual topics in aging were covered, such as dietary restriction (DR), inflammation, stress resistance, homeostasis and proteasome activity, sarcopenia, and neural degeneration. There was also discussion of newer methods, such as microRNAs and genome sequencing, that have been employed to investigate gene expression variance with aging and genetic signatures of longevity. Aging as a field continues to mature, including the following areas: Using a systems approach to tracing conserved pathways across organisms; sharpening definitions of sarcopenia, frailty, and health span; and distinguishing interventions by age tier (early-onset versus late-onset)...
August 2011: Rejuvenation Research
Yi Zang, Li-Fang Yu, Tao Pang, Lei-Ping Fang, Xu Feng, Tie-Qiao Wen, Fa-Jun Nan, Lin-Yin Feng, Jia Li
Neural stem cell differentiation and the determination of lineage decision between neuronal and glial fates have important implications in the study of developmental, pathological, and regenerative processes. Although small molecule chemicals with the ability to control neural stem cell fate are considered extremely useful tools in this field, few were reported. AICAR is an adenosine analog and extensively used to activate AMP-activated protein kinase (AMPK), a metabolic "fuel gauge" of the biological system...
March 7, 2008: Journal of Biological Chemistry
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