13 results on '"Aleman, I."'
Search Results
2. Insulin-like Growth Factor-I and Neuroprotection
- Author
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CARRO, E., primary, TREJO, J.L., additional, FERNANDEZ, S., additional, FERNANDEZ, A.M., additional, and TORRES-ALEMAN, I., additional
- Published
- 2006
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3. Cell-specific expression of insulin/insulin-like growth factor-I receptor hybrids in the mouse brain.
- Author
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Martinez-Rachadell L, Aguilera A, Perez-Domper P, Pignatelli J, Fernandez AM, and Torres-Aleman I
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- Animals, Astrocytes cytology, Brain cytology, Cells, Cultured, Male, Mice, Mice, Inbred C57BL, Microglia cytology, Neurons cytology, Protein Multimerization, Receptor, IGF Type 1 genetics, Receptor, Insulin genetics, Astrocytes metabolism, Brain metabolism, Microglia metabolism, Neurons metabolism, Receptor, IGF Type 1 metabolism, Receptor, Insulin metabolism
- Abstract
Insulin (IR) and insulin-like growth factor I (IGF-IR) receptors share structural homology and can form hybrid heterodimers. While different observations suggest that hybrid receptors are important in physiology and pathology, little is known about their function in the brain. To gain further insight into the role of IR/IGF-IR hybrids in this organ, we analyzed their cellular distribution in the mouse brain. We combined proximity ligation assays (PLA) for IR and IGF-IR, a technique that detects close protein-protein interactions, with immunocytochemistry for brain cell markers to identify IR/IGF-IR hybrids in the major types of brain cells. Intriguingly, while all the types of brain cells analyzed co-express both receptors, only neurons, astroglia, and microglia show readily detectable IR/IGF-IR hybrids. Hybrid PLA signal was negligible in brain endothelial cells and was absent in oligodendrocytes. Hybrids were comparatively more abundant in neurons and peaked after brain development was completed. Cell-specific expression and greater abundance in the adult brain suggests specialized actions of IR/IGF-IR hybrids in this organ, particularly in neurons., (Copyright © 2019 Elsevier Ltd. All rights reserved.)
- Published
- 2019
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4. Exercise and cerebrovascular plasticity.
- Author
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Nishijima T, Torres-Aleman I, and Soya H
- Subjects
- Aging physiology, Animals, Brain cytology, Humans, Insulin-Like Growth Factor I metabolism, Cerebrovascular Circulation physiology, Exercise physiology, Neovascularization, Physiologic physiology, Neuronal Plasticity physiology
- Abstract
Aging impairs cerebrovascular plasticity and subsequently leads cerebral hypoperfusion, which synergistically accelerates aging-associated cognitive dysfunction and neurodegenerative diseases associated with impaired neuronal plasticity. On the other hand, over two decades of researches have successfully demonstrated that exercise, or higher level of physical activity, is a powerful and nonpharmacological approach to improve brain function. Most of the studies have focused on the neuronal aspects and found that exercise triggers improvements in neuronal plasticity, such as neurogenesis; however, exercise can improve cerebrovascular plasticity as well. In this chapter, to understand these beneficial effects of exercise on the cerebral vasculature, we first discuss the issue of changes in cerebral blood flow and its regulation during acute bouts of exercise. Then, how regular exercise improves cerebrovascular plasticity will be discussed. In addition, to shed light on the importance of understanding interactions between the neuron and cerebral vasculature, we describe neuronal activity-driven uptake of circulating IGF-I into the brain., (© 2016 Elsevier B.V. All rights reserved.)
- Published
- 2016
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5. Insulin-like growth factor-1 and central neurodegenerative diseases.
- Author
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Torres Aleman I
- Subjects
- Aging metabolism, Animals, Autophagy physiology, Endoplasmic Reticulum Stress physiology, Humans, Inflammation metabolism, Mice, Oxidative Stress physiology, Rats, Receptor, IGF Type 1 metabolism, Unfolded Protein Response physiology, Central Nervous System Diseases metabolism, Insulin-Like Growth Factor I metabolism, Neurodegenerative Diseases metabolism
- Abstract
The previously undisputed neuroprotective role of insulin-like growth factor 1 (IGF-1) has been challenged by recent observations in IGF-1 receptor (IGF-1R) defective mutants. As new ligand-dependent and ligand-independent roles for IGF-1R are now emerging, new insights into the biologic role of brain IGF-1R and its connection with serum and brain IGF-1 function are urgently required. In the meantime, treatment of specific neurodegenerative diseases with IGF-1 may still be explored using adequate preclinical procedures., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
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6. Emerging roles of insulin-like growth factor-I in the adult brain.
- Author
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Fernandez S, Fernandez AM, Lopez-Lopez C, and Torres-Aleman I
- Subjects
- Adult, Alzheimer Disease metabolism, Animals, Astrocytes cytology, Brain cytology, Cell Proliferation, Endothelium, Vascular metabolism, Humans, Insulin-Like Growth Factor I metabolism, Mice, Astrocytes physiology, Brain blood supply, Brain physiology, Insulin-Like Growth Factor I physiology
- Abstract
All tissues in the body are under the influence of insulin-like growth factor-I (IGF-I). Together with insulin, IGF-I is a key regulator of cell metabolism and growth. IGF-I also acts in the central nervous system, where it affects many different cell populations. In this brief review, we discuss the many roles of IGF-I in the adult brain, and present the idea that diseases affecting the brain will perturb IGF-I activity, although more refined studies at the molecular and cellular level are needed before we can firmly established this possibility. We also suggest that under normal physiological conditions IGF-I may play a significant role in higher brain functions underlying cognition, and may serve a homeostatic role during brain aging. Among newly emerging issues, the effects of IGF-I on non-neuronal cells within the nervous system and their impact in brain physiology and pathology are becoming very important in understanding the biology of this peptide in the brain.
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- 2007
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7. Blockade of the insulin-like growth factor I receptor in the choroid plexus originates Alzheimer's-like neuropathology in rodents: new cues into the human disease?
- Author
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Carro E, Trejo JL, Spuch C, Bohl D, Heard JM, and Torres-Aleman I
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- Aging, Alzheimer Disease cerebrospinal fluid, Alzheimer Disease psychology, Animals, Blotting, Western, Cell Culture Techniques, Choroid Plexus cytology, Epithelial Cells, Glycogen Synthase Kinase 3 metabolism, Green Fluorescent Proteins, Humans, Insulin-Like Growth Factor I deficiency, Maze Learning, Mice, Mice, Inbred C57BL, Mutation, Phosphorylation, Rats, Rats, Wistar, Receptor, IGF Type 1 blood, Signal Transduction, tau Proteins metabolism, Alzheimer Disease metabolism, Choroid Plexus metabolism, Receptor, IGF Type 1 metabolism
- Abstract
The possibility that perturbed insulin/insulin-like growth factor I (IGF-I) signalling is involved in development of late-onset forms of Alzheimer's disease (AD) is gaining increasing attention. We recently reported that circulating IGF-I participates in brain amyloid beta (Abeta) clearance by modulating choroid plexus function. We now present evidence that blockade of the IGF-I receptor in the choroid plexus originates changes in brain that are reminiscent of those found in AD. In rodents, IGF-I receptor impairment led to brain amyloidosis, cognitive disturbance, and hyperphosphorylated tau deposits together with other changes found in Alzheimer's disease such as gliosis and synaptic protein loss. While these disturbances were mostly corrected by restoring receptor function, blockade of the IGF-I receptor exacerbated AD-like pathology in old mutant mice already affected of brain amyloidosis and cognitive derangement. These findings may provide new cues into the causes of late-onset Alzheimer's disease in humans giving credence to the notion that an abnormal age-associated decline in IGF-I input to the choroid plexus may contribute to development of AD in genetically prone subjects.
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- 2006
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8. Therapeutic actions of insulin-like growth factor I on APP/PS2 mice with severe brain amyloidosis.
- Author
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Carro E, Trejo JL, Gerber A, Loetscher H, Torrado J, Metzger F, and Torres-Aleman I
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- Amyloid beta-Peptides metabolism, Amyloidosis complications, Amyloidosis physiopathology, Analysis of Variance, Animals, Behavior, Animal drug effects, Blood-Brain Barrier drug effects, Blood-Brain Barrier physiopathology, Brain Chemistry drug effects, Brain Diseases complications, Brain Diseases physiopathology, Cognition Disorders drug therapy, Cognition Disorders etiology, Disease Models, Animal, Immunohistochemistry methods, Maze Learning drug effects, Mice, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments metabolism, Spatial Behavior drug effects, Amyloid beta-Protein Precursor genetics, Amyloidosis drug therapy, Brain Diseases drug therapy, Insulin-Like Growth Factor I therapeutic use
- Abstract
Transgenic mice expressing mutant forms of both amyloid-beta (Abeta) precursor protein (APP) and presenilin (PS) 2 develop severe brain amyloidosis and cognitive deficits, two pathological hallmarks of Alzheimer's disease (AD). One-year-old APP/PS2 mice with high brain levels of Abeta and abundant Abeta plaques show disturbances in spatial learning and memory. Treatment of these deteriorated mice with a systemic slow-release formulation of insulin-like growth factor I (IGF-I) significantly ameliorated AD-like disturbances. Thus, IGF-I enhanced cognitive performance, decreased brain Abeta load, increased the levels of synaptic proteins, and reduced astrogliosis associated to Abeta plaques. The beneficial effects of IGF-I were associated to a significant increase in brain Abeta complexed to protein carriers such as albumin, apolipoprotein J or transthyretin. Since levels of APP were not modified after IGF-I therapy, and in vitro data showed that IGF-I increases the transport of Abeta/carrier protein complexes through the choroid plexus barrier, it seems that IGF-I favors elimination of Abeta from the brain, supporting a therapeutic use of this growth factor in AD.
- Published
- 2006
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9. Role of serum insulin-like growth factor I in mammalian brain aging.
- Author
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Trejo JL, Carro E, Lopez-Lopez C, and Torres-Aleman I
- Subjects
- Amyloid beta-Peptides metabolism, Animals, Blood-Brain Barrier physiology, Brain blood supply, Hippocampus physiology, Humans, Aging physiology, Brain physiology, Insulin-Like Growth Factor I metabolism, Neurons physiology
- Abstract
Modern societies face new public health challenges associated with an increasingly aging population. Among these, pathological conditions linked to brain aging are paramount. Old age is a risk factor for important neurological impairments such as Alzheimer's disease or stroke. Even healthy elderly people usually present with milder forms of cognitive decline. This is possibly related to less-pronounced brain deficits seen in normal aging, including the shrinkage of neurons and the dense network of neurons and glia in the central nervous system known as the neuropil, a lower neurogenetic rate, impaired angiogenesis or brain accumulation of deleterious compounds. At least in mammals, age is also associated with a decline in insulin-like growth factor-I (IGF-I) levels, a well-known neuroprotective agent. Recently, a relationship between serum IGF-I and "house-keeping" mechanisms in the brain has been evidenced in laboratory rodents. Serum IGF-I increases adult neurogenesis, sustains neuronal health through a variety of fundamental homeostatic mechanisms, participates in brain angiogenesis, contributes to brain beta-amyloid clearance and affects learning and memory. Overall, diminished trophic input resulting from decreasing serum IGF-I levels during aging likely contributes to brain senescence in mammals.
- Published
- 2004
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10. [Modern algorithm for treating pudendal neuralgia: 212 cases and 104 decompressions].
- Author
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Bautrant E, de Bisschop E, Vaini-Elies V, Massonnat J, Aleman I, Buntinx J, de Vlieger J, Di Constanzo M, Habib L, Patroni G, Siboni S, Céas B, Schiby V, and Uglione-Céas M
- Subjects
- Adult, Aged, Aged, 80 and over, Decompression, Surgical methods, Electrophysiology, Female, Humans, Middle Aged, Nerve Compression Syndromes complications, Neuralgia diagnosis, Neuralgia surgery, Peripheral Nerve Injuries, Treatment Outcome, Anal Canal innervation, Neuralgia therapy, Vagina innervation
- Abstract
Clinical signs and symptoms of the pudendal neuralgia are very rich, with a great individual variability. The clinical diagnosis is difficult. It is confirmed or invalidated by the electrophysiologicals tests. Since October 1998 patient selection has been possible using a diagnosis score. Over a four-year period, the diagnosis of pudendal neuralgia was confirmed by electrophysiological investigations in 212 subjects. We rejected 12 patients because of a radiculo-medullary organic etiology. We only describe here cases of women with a peripheral pudendal nerve injury (200 patients). Thirty-eight neuropathies free of canal symptoms (obstetrical, post-traumatic...) were treated by infiltration therapy. The study of a total of 162 canal syndromes showed prevalent injury at the sacro-spino-tuberal ligamental grip which was observed in 68% of the cases, compared to the Alcock canal which was present in only 20% of the cases. One hundred four of these patients underwent surgical decompression via a trans-ischio-rectal approach after negative results of the infiltration therapy. We report here the surgical methodology, the post-op follow-up and the results, which appear quite successful: after one year 86% of the subjects are symptom-free or with a significant reduction of pain.
- Published
- 2003
11. Corticotropin releasing factor (CRF): immunocytochemical localization and radioimmunoassay (RIA).
- Author
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Vigh S, Merchenthaler I, Torres-Aleman I, Sueiras-Diaz J, Coy DH, Carter WH, Petrusz P, and Schally AV
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- Animals, Female, Immunoenzyme Techniques, Male, Rabbits, Radioimmunoassay methods, Rats, Rats, Inbred Strains, Brain Chemistry, Corticotropin-Releasing Hormone analysis
- Published
- 1982
- Full Text
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12. Synthesis and biological properties of ovine corticotropin-releasing factor (CRF).
- Author
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Sueiras-Diaz J, Coy DH, Vigh S, Redding TW, Huang WY, Torres-Aleman I, and Schally AV
- Subjects
- Adrenocorticotropic Hormone metabolism, Animals, Biological Assay, Cells, Cultured, Chromatography, Gel, Chromatography, High Pressure Liquid, Corticotropin-Releasing Hormone pharmacology, Cyanogen Bromide, Dose-Response Relationship, Drug, Pituitary Gland drug effects, Rats, Sheep, Trypsin metabolism, Corticotropin-Releasing Hormone chemical synthesis
- Abstract
The 41-residue sequence of recently identified ovine corticotropin-releasing factor (CRF) was assembled on a benzhydrylamine resin support. Deprotection and cleavage from the resin were accomplished by HF treatment. The crude peptide was purified by gel filtration and reverse-phase, medium pressure, followed by high-performance liquid chromatography (HPLC). In addition to the usual criteria, the homogeneity of the final material, obtained in 7% yield, was assessed by the isolation and examination of cyanogen bromide cleavage and tryptic digestion fragments by HPLC and amino acid analysis. The synthetic 41 amino acid CRF stimulated the release of corticotropin (ACTH) in three in vitro systems: isolated rat pituitary quarters, monolayer cultures of dispersed pituitary cells, and superfused pituitary cells on a column, the responses being related to the log-dose of CRF in the range of 0.05-125 ng/ml. The synthetic peptide also augmented in vivo release of ACTH in rats pretreated with chlorpromazine, morphine, and Nembutal, as assessed by the measurement of serum corticosterone. The data indicates chemical purity and high biological activity of synthetic material.
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- 1982
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13. Synthesis and biological activity of a cyclic pseudohexapeptide analog of somatostatin.
- Author
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Gero TW, Spatola AF, Torres-Aleman I, and Schally AV
- Subjects
- Animals, Chemical Phenomena, Chemistry, Growth Hormone metabolism, Peptide Fragments pharmacology, Protein Conformation, Rats, Somatostatin chemical synthesis, Somatostatin pharmacology, Structure-Activity Relationship, Peptide Fragments chemical synthesis, Somatostatin analogs & derivatives
- Abstract
A cyclic pseudohexapeptide analog of somatostatin, cyclo(Pro psi[ CH2S ]Phe-D-Trp-Lys-Thr-Phe) was synthesized by solid phase methods and diphenylphosphoryl azide ring closure. The resulting crystalline compound possessed 23% of the growth hormone inhibitory activity of the parent tetradecapeptide and approximately 6% of the activity of the all-amide cyclic hexapeptide analog in spite of the absence of one of two postulated intramolecular hydrogen bonds.
- Published
- 1984
- Full Text
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