Serotonin depletion during the postnatal developmental period causes behavioral and cognitive alterations and decreases BDNF level in the brain of rats

2021 ◽  
Author(s):  
Hakimeh Saadati ◽  
Farshid Sadegzadeh ◽  
Nona Sakhaie ◽  
Hamdollah Panahpour ◽  
Mohsen Sagha
Keyword(s):  
Developmental Period ◽  
Bdnf Level ◽  
Serotonin Depletion ◽  
The Brain ◽  
Cognitive Alterations

scholarly journals Oxidative Stress and Cognitive Alterations Induced by Cancer Chemotherapy Drugs: A Scoping Review

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1116
Author(s):  
Omar Cauli
Keyword(s):  
Oxidative Stress ◽  
Cancer Patients ◽  
Repeated Administration ◽  
Caffeic Acid Phenethyl Ester ◽  
Scientific Basis ◽  
Clinical Settings ◽  
Chemotherapy Drugs ◽  
Scientific Attention ◽  
The Brain ◽  
Cognitive Alterations

Cognitive impairment is one of the most deleterious effects of chemotherapy treatment in cancer patients, and this problem sometimes remains even after chemotherapy ends. Common classes of chemotherapy-based regimens such as anthracyclines, taxanes, and platinum derivatives can induce both oxidative stress in the blood and in the brain, and these effects can be reproduced in neuronal and glia cell cultures. In rodent models, both the acute and repeated administration of doxorubicin or adriamycin (anthracyclines) or cisplatin impairs cognitive functions, as shown by their diminished performance in different learning and memory behavioural tasks. Administration of compounds with strong antioxidant effects such as N-acetylcysteine, gamma-glutamyl cysteine ethyl ester, polydatin, caffeic acid phenethyl ester, and 2-mercaptoethane sulfonate sodium (MESNA) counteract both oxidative stress and cognitive alterations induced by chemotherapeutic drugs. These antioxidant molecules provide the scientific basis to design clinical trials in patients with the aim of reducing the oxidative stress and cognitive alterations, among other probable central nervous system changes, elicited by chemotherapy in cancer patients. In particular, N-acetylcysteine and MESNA are currently used in clinical settings and are therefore attracting scientific attention.

DOPAMINE AND SEROTONIN DEPLETION IN THE BRAIN OF MARMOSETS PRENATALLY EXPOSED TO MPTP

1992 ◽  
Vol 3 (Supplement) ◽  
pp. 75
Author(s):  
I PEREZ-OTANO ◽  
M T HERRERO ◽  
M R LUQUIN ◽  
J A OBESO ◽  
J DEL-RIO
Keyword(s):  
Prenatally Exposed ◽  
Serotonin Depletion ◽  
The Brain

scholarly journals Treatment with Growth Hormone (GH) Increased the Metabolic Activity of the Brain in an Elder Patient, Not GH-Deficient, Who Suffered Mild Cognitive Alterations and Had an ApoE 4/3 Genotype

2018 ◽  
Vol 19 (8) ◽  
pp. 2294 ◽  
Author(s):  
Jesús Devesa ◽  
Iria Núñez ◽  
Carlos Agra ◽  
Alejandro Bejarano ◽  
Pablo Devesa
Keyword(s):  
Growth Hormone ◽  
Metabolic Activity ◽  
Cerebral Metabolism ◽  
Verbal Learning ◽  
Pet Scan ◽  
Positive Effects ◽  
And Behavior ◽  
Knowledge Memory ◽  
The Brain ◽  
Cognitive Alterations

(1) Background: We analyzed, using PET-SCAN and cognitive tests, how growth hormone (GH) could act in the brain of an older woman, not deficient in GH, who showed mild cognitive alterations (MCI) and had a genotype of ApoE 4/3 and familial dyslipidemia. (2) Methods: After performing a first psychometric study (TAVEC verbal learning test), the metabolic activity of brain structures related to knowledge, memory, and behavior was analyzed using 18-F fluorodeoxyglucose PET-SCAN. The patient was then treated with GH (0.4 mg/day, subcutaneous) for three weeks and on the last day under this treatment, a new PET-SCAN was performed. One month after beginning treatment with GH, a new TAVEC test was performed. (3) Results: GH administration normalized the cognitive deficits observed in the first psychometric test and significantly (p < 0.025) increased the metabolic activity in practically all brain cortical areas, specifically in the left hippocampus and left amygdala, although not in the left parahippocampus. (4) Conclusions: This study demonstrates for the first time the positive effects of GH on cerebral metabolism in a patient without GH deficiency, recovering the function of affected areas related to knowledge, memory, and behavior in an elderly patient with MCI.

Alterations in the monoamines and the synthesizing enzymes in the postnatal developmental period of the brain of Spr-/- mice

2010 ◽  
Vol 68 ◽  
pp. e82
Author(s):  
Daigo Homma ◽  
Hirofumi Tokuoka ◽  
Setsuko Katoh ◽  
Hiroshi Ichinose
Keyword(s):  
Developmental Period ◽  
The Brain

scholarly journals Brain-derived neurotrophic factor as a potential therapeutic tool in the treatment of nervous system disorders

2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurotrophic Factor ◽  
Intracellular Transport ◽  
Brain Derived Neurotrophic Factor ◽  
Nerve Cells ◽  
The Body ◽  
Bdnf Level ◽  
The Central Nervous System ◽  
The Brain

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.

scholarly journals Comparison of Brain-derived Neurotrophic Factor Level in Depressed Patients Treated with Fluoxetine and Sertraline

2021 ◽  
Vol 9 (T3) ◽  
pp. 311-315
Author(s):  
Sonny Teddy Lisal ◽  
Nur Aeni M. A. Fattah ◽  
Rahmawati Nur Indah ◽  
Saidah Syamsuddin
Keyword(s):  
Rating Scale ◽  
Dropping Out ◽  
Factor Level ◽  
Bdnf Level ◽  
Consecutive Sampling ◽  
Neuronal Growth Factor ◽  
Dsm V ◽  
Before And After ◽  
Synaptic Formation ◽  
The Brain

Background: The Brain-Derived NeurotrophicFactor (BDNF) is the main neuronal growth factor in the brain that regulates neurogenesis, neuronal maturity, synaptic formation and plasticity. Studies showed BDNF level decreased in depression and the administration of anti depressant drugs increased BDNF level. In this study, we used fluoxetine and sertraline, which are Selective Serotonin Reuptake Inhibitor (SSRI) but had a different mechanism in influencing the BDNF levels. The purpose of this study was to compare the effect of fluoxetine and sertraline administration tothe BDNF level in depressed subjects. This study was conducted at Wahidin Sudirohusodo Hospital, Makassar, Indonesia and its affiliates from January to February 2019. Twenty outpatient subjects were diagnosed with depression based on DSM-V. The subjects were either antidepressant naïve, or dropping out of antidepressant therapy for at least 3 months since the last administration. Blood samples from each subject were taken by consecutive sampling, and BDNF levels were analyzed before and after administration of fluoxetine and sertraline for six weeks. Also, Hamilton Depression Rating Scale (HDRS) scores are measured before and after administration. The BDNF serum was significantly increased by 100.6% (p<0,001) from the baseline level in the fluoxetine group and 75.4% in the sertraline group. HDRS score was decreased by39.5%  (p<0,001) in the fluoxetine group and 30.1% in the sertraline group after six weeks of administration. This study suggests that fluoxetine was superior to sertraline in increasing the BDNF level in depression.

scholarly journals Relationship Between Brain-Derived Neurotrofic Factor (Bdnf) and Sleep on Depression: A Critical Review

2017 ◽  
Vol 13 (1) ◽  
pp. 213-219 ◽  
Author(s):  
Bárbara C. Monteiro ◽  
Suzana Monteiro ◽  
Maristela Candida ◽  
Nathalia Adler ◽  
Flavia Paes ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Critical Review ◽  
Depressive Disorders ◽  
Poor Sleep ◽  
Poor Sleep Quality ◽  
Bdnf Level ◽  
Low Levels ◽  
Impaired Sleep ◽  
Dopaminergic Pathways ◽  
The Brain

The Brain-Derived Neurotrofic Factor (BDNF) is one of the most important neurotrophins in the brain and it is suggested influences the activity of the serotonergic, noradrenergic and dopaminergic pathways. In the last few years, it has been hypothesized that BDNF level is related with depression and sleep. Several studies show that depressive subjects present low levels of BDNF in the brain. Poor sleep quality is also related with alterations in the BDNF concentration. Some authors argue that most of the cases show that impaired sleep quality increases the stress and, consequently, the vulnerability to depressive disorders, suggesting that there is a relationship between sleep, depression and BDNF levels.

scholarly journals Role of c-Jun N-Terminal Kinases (JNKs) in Epilepsy and Metabolic Cognitive Impairment

2019 ◽  
Vol 21 (1) ◽  
pp. 255 ◽  
Author(s):  
Oriol Busquets ◽  
Miren Ettcheto ◽  
Amanda Cano ◽  
Patricia R. Manzine ◽  
Elena Sánchez-Lopez ◽  
...  
Keyword(s):  
Potential Role ◽  
Regulatory Function ◽  
Neuroprotective Effects ◽  
Peripheral Tissues ◽  
Therapeutic Value ◽  
Jnk Inhibitors ◽  
The Brain ◽  
Cognitive Alterations ◽  
Synthetic Small Molecule

Previous studies have reported that the regulatory function of the different c-Jun N-terminal kinases isoforms (JNK1, JNK2, and JNK3) play an essential role in neurological disorders, such as epilepsy and metabolic-cognitive alterations. Accordingly, JNKs have emerged as suitable therapeutic strategies. In fact, it has been demonstrated that some unspecific JNK inhibitors exert antidiabetic and neuroprotective effects, albeit they usually show high toxicity or lack therapeutic value. In this sense, natural specific JNK inhibitors, such as Licochalcone A, are promising candidates. Nonetheless, research on the understanding of the role of each of the JNKs remains mandatory in order to progress on the identification of new selective JNK isoform inhibitors. In the present review, a summary on the current gathered data on the role of JNKs in pathology is presented, as well as a discussion on their potential role in pathologies like epilepsy and metabolic-cognitive injury. Moreover, data on the effects of synthetic small molecule inhibitors that modulate JNK-dependent pathways in the brain and peripheral tissues is reviewed.

scholarly journals Obesity and Age-Related Changes in the Brain of the Zucker Lepr fa/fa Rats

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1356 ◽  
Author(s):  
Daniele Tomassoni ◽  
Ilenia Martinelli ◽  
Michele Moruzzi ◽  
Maria Vittoria Micioni Di Bonaventura ◽  
Carlo Cifani ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Transporter Protein ◽  
Age Related ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Immunohistochemical Techniques ◽  
The Brain ◽  
Cognitive Alterations

Metabolic syndrome (MetS) is an association between obesity, dyslipidemia, hyperglycemia, hypertension, and insulin resistance. A relationship between MetS and vascular dementia was hypothesized. The purpose of this work is to investigate brain microanatomy alterations in obese Zucker rats (OZRs), as a model of MetS, compared to their counterparts lean Zucker rats (LZRs). 12-, 16-, and 20-weeks-old male OZRs and LZRs were studied. General physiological parameters and blood values were measured. Immunochemical and immunohistochemical techniques were applied to analyze the brain alterations. The morphology of nerve cells and axons, astrocytes and microglia were investigated. The blood–brain barrier (BBB) changes occurring in OZRs were assessed as well using aquaporin-4 (AQP4) and glucose transporter protein-1 (GLUT1) as markers. Body weight gain, hypertension, hyperglycemia, and hyperlipidemia were found in OZRs compared to LZRs. In the frontal cortex and hippocampus, a decrease of neurons was noticeable in the older obese rats in comparison to their age-matched lean counterparts. In OZRs, a reduction of neurofilament immunoreaction and gliosis was observed. The BBB of older OZRs revealed an increased expression of AQP4 likely related to the development of edema. A down-regulation of GLUT1 was found in OZRs of 12 weeks of age, whereas it increased in older OZRs. The behavioral analysis revealed cognitive alterations in 20-week-old OZRs. Based on these results, the OZRs may be useful for understanding the mechanisms through which obesity and related metabolic alterations induce neurodegeneration.

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