G-CSF rescues the memory impairment of animal models of Alzheimer's disease

Tsai, Kuen Jer; Tsai, Yueh Chiao; Shen, Che Kun James

doi:10.1084/jem.20062481

Cited by 138 publications

(99 citation statements)

References 30 publications

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“…Numerous reports have described the efficacy of G-CSF in animal models of different neurological diseases including stroke (Schabitz et al, 2003;Schneider et al, 2005;KomineKobayashi et al, 2006;Solaroglu et al, 2006;Minnerup et al, 2008), Parkinson's disease (Cao et al, 2006;Meuer et al, 2006), and Alzheimer's disease (Tsai et al, 2007). These studies confirm G-CSF as a neurotrophic factor, and ascertained its role in neuroprotection and neuroregeneration relevant to the most prominent neurodegenerative diseases.…”

Section: Introductionsupporting

confidence: 54%

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Diederich¹,

Sevimli²,

Dörr³

et al. 2009

J. Neurosci.

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Granulocyte-colony stimulating factor (G-CSF) is a hematopoietic growth factor that controls proliferation and differentiation of neural stem cells. Although recent studies have begun to explore G-CSF-related mechanisms of action in various disease models, little is known about its function in the healthy brain. In the present study, the effect of G-CSF deficiency on memory formation and motor skills was investigated. The impact of G-CSF deficiency on the structural integrity of the hippocampus was evaluated by analyzing the generation of doublecortin-expressing cells, the amount of bromodeoxyurine-labeled cells, the dendritic complexity in hippocampal neurons, the binding densities of NMDA and GABA A receptors and the induction of long-term potentiation (LTP). G-CSF deficiency caused a disruption in memory formation and in the development of motor skills. These impairments were associated with reduced ligand binding densities of NMDA receptors in hippocampal subfields CA3 and the dentate gyrus. The reduced excitation was potentiated by increased ligand binding densities of GABA A receptors resulting in a relative shift in favor of inhibition and impaired behavioral performance. These alterations were accompanied by impaired induction of LTP in the CA1 region. Moreover, G-CSF deficiency led to decreased dendritic complexity in hippocampal neurons in the dentate gyrus and the CA1 region. G-CSF deficiency also caused a reduction of neuronal precursor cells in the dentate gyrus. These findings confirm G-CSF as an essential neurotrophic factor, and point to a role in the proliferation, differentiation and functional integration of neural cells necessary for the structural and functional integrity of the hippocampal formation.

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Section: Introductionsupporting

confidence: 54%

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Diederich¹,

Sevimli²,

Dörr³

et al. 2009

J. Neurosci.

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“…In animal models of AD, i.e., β-amyloid protein-expressing transgenic and AF64A-injected mice, 25-30% decrease in brain ACh resulted in severe impairment of learning and memory function (Yamazaki et al, 1991;Abe et al, 1993;Tsai et al, 2007;Bessho et al, 2008). During aging, brain atrophy and malfunction of cholinergic nervous system occur, leading to cognitive defi cit.…”

Section: Discussionmentioning

confidence: 99%

Improving Effect of Silk Peptides on the Cognitive Function of Rats with Aging Brain Facilitated by D-Galactose

Park¹,

Lee²,

Choi³

et al. 2011

Biomolecules and Therapeutics

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“…A decrease in G-CSF blood levels in early AD patients has been reported by Laske et al, with no data available for the CSF or brain level of this growth factor (188). Tsai et al have reported a significant cognitive improvement in transgenic mice models of AD after 5 days of subcutaneous injection of G-CSF (189). They also reported that G-CSF administration induced neurogenesis around Aβ aggregates in these acute and chronic animal models of Aβ-driven AD.…”

Section: Granulocyte-colony Stimulating Factormentioning

confidence: 93%

Alzheimer’s Disease: Dawn of a New Era?

et al. 2017

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Alzheimer’s disease (AD) is an irreversible neurodegenerative disease characterized by a progressive decline in cognition and memory, leading to significant impairment in daily activities and ultimately death. It is the most common cause of dementia, the prevalence of which increases with age; however, age is not the only predisposing factor. The pathology of this cognitive impairing disease is still not completely understood, which has limited the development of valid therapeutic options. Recent years have witnessed a wide range of novel approaches to combat this disease, so that they greatly increased our understanding of the disease and of the unique drug development issues associated with this disease. In this paper, we provide a brief overview of the history, the clinical presentation and diagnosis, and we undertake a comprehensive review of the various approaches that have been brought to clinical trials in recent years, including immunotherapeutic approaches, tau-targeted strategies, neurotransmitter-based therapies, neurotropic and hematopoietic growth factors, and antioxidant therapies, trying to highlight the lessons learned from these approaches. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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G-CSF rescues the memory impairment of animal models of Alzheimer's disease

Cited by 138 publications

References 30 publications

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Improving Effect of Silk Peptides on the Cognitive Function of Rats with Aging Brain Facilitated by D-Galactose

Alzheimer’s Disease: Dawn of a New Era?

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