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

  title={Insulin growth factor binding protein 7 is a novel target to treat dementia},
  author={Hope Yao Agbemenyah and Roberto Carlos Ag{\'i}s-Balboa and Susanne Burkhardt and Ivana Delalle and Andr{\'e} Fischer},
  journal={Neurobiology of Disease},
Insulin-like growth factor 5 associates with human Aß plaques and promotes cognitive impairment
It is shown that Insulin-like Growth Factor Binding Protein 5 (Igfbp5), an inhibitory binding protein for insulin-like growth factor 1 (IGf-1) accumulates in hippocampal pyramidal neurons and in amyloid plaques in brains of Alzheimer patients.
Alzheimer amyloid peptide aβ42 regulates gene expression of transcription and growth factors.
The pathogenesis of Alzheimer's disease (AD) is characterized by the aggregation of amyloid-β (Aβ) peptides leading to deposition of senile plaques and a progressive decline of cognitive functions,
Insulin-Like Growth Factor 2 As a Possible Neuroprotective Agent and Memory Enhancer—Its Comparative Expression, Processing and Signaling in Mammalian CNS
This work provides a detailed description of Igf2 mRNA expression regulation and pre-pro-IGF-2 protein processing in different species, and describes three different receptors able to bind IGF-2.
Insulin-like growth factor-1 and insulin-like growth factor binding protein 3 and risk of postoperative cognitive dysfunction
Logistic regression analysis revealed that lower preoperative IGF-1 level and elderly patients increased the odds of POCD, and down-regulation of circulating IGF- 1 level may be involved in the mechanism of 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
The rapidly growing world of IGF2 in cognitive neuroscience is reviewed and 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 is introduced.
DNA Modifications and Alzheimer's Disease.
This chapter discusses the current state of play for research into DNA modifications in AD, with the most well studied being 5-methylcytosine (5-mC), and focuses on recent epigenome-wide association studies (EWAS) in human AD, using microarray technology.
Altered insulin-like growth factor-2 signaling is associated with psychopathology and cognitive deficits in patients with schizophrenia
It is demonstrated that serum IGF-2 was significantly correlated with negative and cognitive symptoms in patients with schizophrenia, suggesting that altered IGF- 2 signaling may be implicated in the psychopathology and cognitive deficits in schizophrenia.
Opening up the DNA methylome of dementia
This review provides an in-depth summary of the current knowledge about DNA methylation in dementia, focusing exclusively on the analyses performed in human brain.
Urine-Based Biomarkers for Alzheimer's Disease Identified Through Coupling Computational and Experimental Methods.
SPP1, GSN, and IGFBP7 were found to be differentially expressed in the urine of AD patients and found that they were involved in AD pathophysiology and might serve as new urine biomarkers for AD.
Insulin-like Growth Factor 1 Signaling in Mammalian Hearing
The contribution of the IGF system to the understanding of the molecular and genetic basis of human hearing loss is reviewed by describing the expression patterns of theIGF system in the mammalian inner ear; downstream signaling of IGF-1 in the hearing organ; and human mutations in these genes causing hearing loss.


Insulin-like growth factor-I and insulin-like growth factor binding protein-3 in Alzheimer's disease.
A significant association between low IGF-I and IGFBP-3 serum levels and AD in men, but not in women is reported; this is the first study of its kind to report this association.
Serum insulin-like growth factor I regulates brain amyloid-β levels
IGF-I treatment of mice overexpressing mutant amyloid markedly reduces their brain Aβ burden, and it is considered that circulating IGF-I is a physiological regulator of brain amyloids levels with therapeutic potential.
Mechanisms Underlying Insulin Deficiency-Induced Acceleration of β-Amyloidosis in a Mouse Model of Alzheimer's Disease
These findings provide a mechanistic foundation for a link between diabetes and AD by demonstrating that insulin deficiency may change APP processing to favor β-amyloidogenesis via the translational upregulation of BACE1 in combination with elevations in its substrate, APP.
Reduced IGF-1 Signaling Delays Age-Associated Proteotoxicity in Mice
Neuronal IGF‐1 resistance reduces Aβ accumulation and protects against premature death in a model of Alzheimer's disease
  • S. Freude, M. Hettich, M. Schubert
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2009
It is shown that IRS‐2 deficiency in Tg2576 mice completely reverses premature mortality in T g2576 females and delays β‐amyloid (Aβ) accumulation, and impaired IGF‐1/IRS‐2 signaling prevents premature death and delays amyloid accumulation in a model of AD.
Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline.
Brain insulin resistance appears to be an early and common feature of AD, a phenomenon accompanied by IGF-1 resistance and closely associated with IRS-1 dysfunction potentially triggered by Aβ oligomers and yet promoting cognitive decline independent of classic AD pathology.
IGF-I and the aging mammalian brain
Impaired neuronal insulin signaling precedes Aβ42 accumulation in female AβPPsw/PS1ΔE9 mice.
The results suggest a possible early role for insulin signaling impairment leading to amyloid accumulation in AβPPsw/PS1ΔE9 mice.