Neurotrophic Factors and Their Receptors Are Altered by the Mere Partial IGF-1 Deficiency

Castilla‐Cortázar, Inma; Iturrieta, Ignacio; García‐Magariño, Mariano; Puche, Juan Enrique; Martín-Estal, Irene; Aguirre, Gabriel A.; Femat-Roldán, Giovana; Cantú-Martínez, Leonel; Muñoz, Úrsula

doi:10.1016/j.neuroscience.2019.01.041

Cited by 9 publications

(5 citation statements)

References 84 publications

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“…Consistently, these IGF-1 deficient mice have an alteration in the blood-brain barrier due to a distorted genetic expression of extracellular matrix and intercellular adhesion proteins (unpublished data). Furthermore, IGF-1 deficiency showed in this experimental model, an altered gene expression pattern encoding neurotrophic factors and their receptors [130]. While most of the results found in the literature have been discovered using in vitro studies, other were discovered using animal models of CNS injury or IGF-1 deficiency.…”

Section: Igf-1 Actions In the Central Nervous Systemmentioning

confidence: 72%

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

et al. 2020

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Parkinson's disease (PD) is a neurodegenerative disorder that results in the death of dopaminergic neurons within the substantia nigra pars compacta and the reduction in dopaminergic control over striatal output neurons, leading to a movement disorder most commonly characterized by akinesia or bradykinesia, rigidity and tremor. Also, PD is less frequently depicted by sensory symptoms (pain and tingling), hyposmia, sleep alterations, depression and anxiety, and abnormal executive and working memory related functions. On the other hand, insulin-like growth factor 1 (IGF-1) is an endocrine, paracrine and autocrine hormone with several functions including tissue growth and development, insulin-like activity, proliferation, pro-survival, anti-aging, antioxidant and neuroprotection, among others. Herein this review tries to summarize all experimental and clinical data to understand the pathophysiology and development of PD, as well as its clear association with IGF-1, supported by several lines of evidence: (1) IGF-1 decreases with age, while aging is the major risk for PD establishment and development; (2) numerous basic and translational data have appointed direct protective and homeostasis IGF-1 roles in all brain cells; (3) estrogens seem to confer women strong protection to PD via IGF-1; and (4) clinical correlations in PD cohorts have confirmed elevated IGF-1 levels at the onset of the disease, suggesting an ongoing compensatory or "fight-to-injury" mechanism.

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Section: Igf-1 Actions In the Central Nervous Systemmentioning

confidence: 72%

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

et al. 2020

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“…Indeed, IGF-1 signaling itself was reduced in hNSC treated versus 5XFAD animals ( Supplementary Figure S17C , there was minimal contamination of transcriptomic data by human mRNA and therefore IGF-1 expression from hNSCs would not be detected here). IGF-1 may also directly downregulate expression of the CNTN1 receptor NRCAM ( Castilla-Cortazar et al, 2019 ), thus impacting the CNTN1-NRCAM interaction. hNSCs may also act by additional paracrine biochemical mediators that remain to be revealed.…”

Section: Discussionmentioning

confidence: 99%

Human neural stem cells restore spatial memory in a transgenic Alzheimer’s disease mouse model by an immunomodulating mechanism

Chen,

Noureldein,

McGinley

et al. 2023

Front. Aging Neurosci.

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IntroductionStem cells are a promising therapeutic in Alzheimer’s disease (AD) given the complex pathophysiologic pathways involved. However, the therapeutic mechanisms of stem cells remain unclear. Here, we used spatial transcriptomics to elucidate therapeutic mechanisms of human neural stem cells (hNSCs) in an animal model of AD.MethodshNSCs were transplanted into the fimbria fornix of the hippocampus using the 5XFAD mouse model. Spatial memory was assessed by Morris water maze. Amyloid plaque burden was quantified. Spatial transcriptomics was performed and differentially expressed genes (DEGs) identified both globally and within the hippocampus. Subsequent pathway enrichment and ligand-receptor network analysis was performed.ResultshNSC transplantation restored learning curves of 5XFAD mice. However, there were no changes in amyloid plaque burden. Spatial transcriptomics showed 1,061 DEGs normalized in hippocampal subregions. Plaque induced genes in microglia, along with populations of stage 1 and stage 2 disease associated microglia (DAM), were normalized upon hNSC transplantation. Pathologic signaling between hippocampus and DAM was also restored.DiscussionhNSCs normalized many dysregulated genes, although this was not mediated by a change in amyloid plaque levels. Rather, hNSCs appear to exert beneficial effects in part by modulating microglia-mediated neuroinflammation and signaling in AD.

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“…There are three major families of NTFs: the neurotrophin family including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4; the glial-cell derived neurotrophic factor (GDNF) family; and the neuropoietic or interleukin-6 family. These NTFs are potential treatments for neurological diseases due to their regenerative capabilities [ 125 , 126 , 127 , 128 ].…”

Section: Alcohol and Neuroinflammatory Mechanism Activated In Sbimentioning

confidence: 99%

Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation

Thangameeran,

Wang,

Liew

et al. 2024

Life

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The intricate relationship between alcohol consumption and intracerebral hemorrhage (ICH) presents a nuanced field of study, especially concerning the dose-dependent impact on secondary brain injury (SBI). Recognizing the established risks associated with heavy drinking, this review delves deeper into the less understood territories of low to moderate alcohol consumption. By systematically analyzing recent studies, we uncover critical insights into how varying alcohol intake levels modulate ICH risk through mechanisms such as microglial activation, oxidative stress, and the protective potential of polyphenols. This analysis extends beyond the hypertensive effects of heavy alcohol use to explore the complex molecular pathophysiology involved in alcohol-related ICH. Our findings indicate that while heavy alcohol use unequivocally exacerbates ICH risk, moderate consumption and its associated polyphenols may offer neuroprotective effects against SBI, albeit within a finely balanced threshold. This review highlights the significant gaps in current understanding and underscores the urgent need for targeted research to elucidate these complex interactions. Through this comprehensive examination, we aim to inform more nuanced public health policies and intervention strategies, taking into account the diverse effects of alcohol consumption on ICH risk.

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Neurotrophic Factors and Their Receptors Are Altered by the Mere Partial IGF-1 Deficiency

Cited by 9 publications

References 84 publications

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

Is insulin-like growth factor-1 involved in Parkinson’s disease development?

Human neural stem cells restore spatial memory in a transgenic Alzheimer’s disease mouse model by an immunomodulating mechanism

Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation

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