Insulin growth factor binding protein 7 is a novel target to treat dementia

Agbemenyah, Hope Yao; Agís‐Balboa, Roberto Carlos; Burkhardt, Susanne; Delalle, Ivana; Fischer, André

doi:10.1016/j.nbd.2013.09.011

Cited by 45 publications

(38 citation statements)

References 55 publications

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“…The mammalian genome encodes seven IGFBPs that are named IGFBP1 to IGFBP7. IGFBP7, a protein that attenuates the function of insulin-like peptide (ILP) signaling, is a critical regulator of memory consolidation [16], a specific up-regulation of which was seen not only in the hippocampus of APP mice and AD patients [16] but also in blood serum of AD patients [30]. Increased IGFBP7 levels mediate cellular senescence and apoptosis [31] and correlated with decreased p-Akt levels, which is a sensitive intracellular measure of ILP signaling [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

The change of circulating insulin like growth factor binding protein 7 levels may correlate with postoperative cognitive dysfunction

Jiang

Chen

Liang

et al. 2015

Neuroscience Letters

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Section: Discussionmentioning

confidence: 99%

The change of circulating insulin like growth factor binding protein 7 levels may correlate with postoperative cognitive dysfunction

Jiang

Chen

Liang

et al. 2015

Neuroscience Letters

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“…In addition, they recently demonstrated the increases of IGFBP7 in the hippocampus of a mouse model for AD and in the prefrontal cortex of AD patients (Agbemenyah et al, 2014). Intrahippocampal injection of IGFBP7 impaired memory consolidation in wild mice, whereas that of neutralizing antibodies for IGFBP7 ameliorated associative memory disturbance in APP mice.…”

Section: Igf2 Is Essential For Fear Extinctionmentioning

confidence: 99%

Emerging evidence of insulin-like growth factor 2 as a memory enhancer: a unique animal model of cognitive dysfunction with impaired adult neurogenesis

Iwamoto¹,

Ouchi²

2014

Reviews in the Neurosciences

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In the current aging society, cognitive dysfunction is one of the most serious issues that should be urgently resolved. It also affects a wide range of age groups harboring neurological and psychiatric disorders, such as Alzheimer's disease and schizophrenia. Although the molecular mechanism of memory impairment still remains to be determined, neuronal loss and dysfunction has been revealed to mainly attribute to its pathology. The discovery of neural stem cells in the adult brain that are proliferating and able to generate functional neurons has given rise to the idea that neuronal loss could be rescued by manipulating endogenous neural progenitor and stem cells. To this end, we must characterize them in detail and their developmental programming must be better understood. A growing body of evidence has indicated that insulin-like peptides are involved in learning and memory and maintenance of neural progenitor and stem cells, and clinical trials of insulin as a memory enhancer have begun. In contrast to the expectation of insulin and IGF1, the roles of IGF2 in cognitive ability have been poorly understood. However, recent evidence demonstrated in rodents suggests that IGF2 may play a pivotal role in adult neurogenesis and cognitive function. Here, we would like to review the rapidly growing world of IGF2 in cognitive neuroscience and introduce the evidence that its deficit is indeed involved in the impairment of the hippocampal neurogenesis and cognitive dysfunction in the model mouse of 22q11.2 deletion syndrome, which deletes Dgcr8, a critical gene for microRNA processing.

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“…Interestingly, it has been demonstrated in mice that IGF2/IGFBP7 signalling regulates fear extinction via an upregulation of IGF2 and downregulation of IGFBP7, which promotes survival of 17–19-day-old newborn hippocampal neurons [97]. Both IGF2 and IGFBP7 genes are regulated via DNA methylation and other epigenetic mechanisms [91, 98]. This signalling pathway might have potential as therapeutic target for PTSD, although this possibility will need to be studied further.…”

Section: Main Textmentioning

confidence: 99%

“…For example, in this context, there is evidence showing that childhood abuse induces differential DNA methylation and gene expression patterns in PTSD patients compared to PTSD patients without childhood abuse [110]. IGFBP7, one of the seven IGFBPs identified in the mammalian genome that is used to transport and regulate the bioavailability of IGF1 and IGF2, is deregulated in PTSD and dementia via Igfbp7 promoter DNA methylation in mouse and human brains [91, 98]. In this context, epigenetic pharmacology emerges as an appealing alternative to treat multifactorial diseases with deregulation in multiple signalling pathways in the framework of personalized medicine [111].…”

Section: Main Textmentioning

confidence: 99%

Epigenetic mechanisms during ageing and neurogenesis as novel therapeutic avenues in human brain disorders

et al. 2017

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Ageing is the main risk factor for human neurological disorders. Among the diverse molecular pathways that govern ageing, epigenetics can guide age-associated decline in part by regulating gene expression and also through the modulation of genomic instability and high-order chromatin architecture. Epigenetic mechanisms are involved in the regulation of neural differentiation as well as in functional processes related to memory consolidation, learning or cognition during healthy lifespan. On the other side of the coin, many neurodegenerative diseases are associated with epigenetic dysregulation. The reversible nature of epigenetic factors and, especially, their role as mediators between the genome and the environment make them exciting candidates as therapeutic targets. Rather than providing a broad description of the pathways epigenetically deregulated in human neurological disorders, in this review, we have focused on the potential use of epigenetic enzymes as druggable targets to ameliorate neural decline during normal ageing and especially in neurological disorders. We will firstly discuss recent progress that supports a key role of epigenetic regulation during healthy ageing with an emphasis on the role of epigenetic regulation in adult neurogenesis. Then, we will focus on epigenetic alterations associated with ageing-related human disorders of the central nervous system. We will discuss examples in the context of psychiatric disorders, including schizophrenia and posttraumatic stress disorders, and also dementia or Alzheimer’s disease as the most frequent neurodegenerative disease. Finally, methodological limitations and future perspectives are discussed.

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Insulin growth factor binding protein 7 is a novel target to treat dementia

Cited by 45 publications

References 55 publications

The change of circulating insulin like growth factor binding protein 7 levels may correlate with postoperative cognitive dysfunction

The change of circulating insulin like growth factor binding protein 7 levels may correlate with postoperative cognitive dysfunction

Emerging evidence of insulin-like growth factor 2 as a memory enhancer: a unique animal model of cognitive dysfunction with impaired adult neurogenesis

Epigenetic mechanisms during ageing and neurogenesis as novel therapeutic avenues in human brain disorders

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