Nutritional Aspects of Down's Syndrome with Special Reference to the Nervous System

1984 ◽  
Vol 145 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Peter E. Sylvester
Keyword(s):  
Nervous System ◽  
Trace Metals ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Pathological Changes ◽  
Age Related ◽  
Mature Brain ◽  
The Brain ◽  
With Memory

SummaryMultiple deficiencies of vitamins and trace metals have been demonstrated in Down's syndrome. The picture is complex, especially since not all individuals are affected equally. Deficiencies are not age-related, but appear to be lifelong. The brain in Downs's syndrome does not develop adequately; one area, the hippocampus, which is concerned with memory, is poorly developed and is also involved in the pathological changes of Alzheimer's disease. The role of nutrients is discussed in relation to damage to the mature brain, and to the ageing process.

scholarly journals Role of Microglia in Age-Related Changes to the Nervous System

2009 ◽  
Vol 9 ◽  
pp. 1061-1071 ◽  
Author(s):  
David R. Brown
Keyword(s):  
Nervous System ◽  
Cognitive Decline ◽  
Neurodegenerative Disease ◽  
Neuronal Death ◽  
Large Population ◽  
Neuronal Loss ◽  
Age Related ◽  
The Brain ◽  
Age Related Changes

Microglia play a curious role in the nervous system. Their role is intrinsically protective and supportive, but during neurodegenerative disease, it is well established that microglia play a significant role in the initiation of neuronal death. Microglia, like neurons, show age-related changes that could potentially alter their behavior. While extreme changes to a large population of microglia cause dramatic neuronal loss in neurodegeneration, during normal aging, subtle changes not unlike those seen in the disease state could potentially contribute to a more gradual neuronal loss that could contribute to the cognitive decline seen in the aging population. This review provides illustrations of what is known about the role of microglia in neurodegeneration and makes suggestions about the role of microglia in age-related changes to the brain.

scholarly journals The Role of Neuropeptide Y in the Nucleus Accumbens

2021 ◽  
Vol 22 (14) ◽  
pp. 7287
Author(s):  
Masaki Tanaka ◽  
Shunji Yamada ◽  
Yoshihisa Watanabe
Keyword(s):  
Nervous System ◽  
Nucleus Accumbens ◽  
Neuropeptide Y ◽  
Emotional Behavior ◽  
Characteristic Functions ◽  
Receptor Subtypes ◽  
Neuroendocrine Mechanisms ◽  
Fear And Anxiety ◽  
The Brain

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.

scholarly journals Activation of central 5-HT2A receptor in brain inhibited the seizure-induced respiratory arrest in the DBA/1 mouse SUDEP model

2020 ◽  
Author(s):  
Yue Shen ◽  
HaiXiang Ma ◽  
XiTing Lian ◽  
LeYuan Gu ◽  
Qian Yu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Drug Resistance ◽  
Nervous System ◽  
Underlying Mechanism ◽  
Respiratory Arrest ◽  
Acoustic Stimulation ◽  
Unexpected Death ◽  
Anti Epileptic Drug ◽  
The Brain

AbstractSudden unexpected death in epilepsy (SUDEP) is the fatal cause leading to the death of epilepsy patients with anti-epileptic drug resistance. However, the underlying mechanism of SUDEP remains to be elusive. Our previous study demonstrated that enhancement of serotonin (5-HT) synthesis by intraperitoneal (IP) injection of 5-hydroxytryptophan in brain significantly reduced the incidence of seizure-induced respiratory arrest (S-IRA) in DBA/1 mice SUDEP models. Given that 5-HT2A receptor (5-HT2AR) acts an important role in mediating respiration system in brain, we hypothesized that 5-HT2AR is of great significance to modulate S-IRA and SUDEP. To test this hypothesis, we examined whether the decreased incidence S-IRA evoked by either acoustic stimulation or PTZ by blocking 5-HT2AR by administration with ketanserin (KET), a selective antagonist of 5HT2AR, in DBA/1 mice SUDEP models to test the role of 5-HT2AR modulating S-IRA. Our results suggested that the decreased incidence of S-IRA by 5-Hydroxytryptophan (5-HTP), a precursor for central nervous system (CNS) serotonin (5-HT) synthesis, was significantly reversed by IP and intracerebroventricularly (ICV) injection of ketanserin in our models. Thus, our data suggested that 5-HT2AR in the brain may be a potential and specific target to prevent SUDEP.

P01.18 Role of pro-inflammatory cytokines in down's syndrome

2000 ◽  
Vol 15 (S2) ◽  
pp. 325s-325s
Author(s):  
M.G. Carta ◽  
M.C. Hardoy ◽  
P.E. Manconil ◽  
P. Serra ◽  
A. Barrancal ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Pro Inflammatory Cytokines

scholarly journals Useful Effects of Melatonin in Peripheral Nerve Injury and Development of the Nervous System

2017 ◽  
Vol 12 (01) ◽  
pp. e1-e6 ◽  
Author(s):  
Yigit Uyanikgil ◽  
Turker Cavusoglu ◽  
Kubilay Kılıc ◽  
Gurkan Yigitturk ◽  
Servet Celik ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Nervous System ◽  
Peripheral Nerve ◽  
Peripheral Nerve Injury ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
High Efficacy ◽  
Nerve Injuries ◽  
Age Related

This review summarizes the role of melatonin (MLT) in defense against toxic-free radicals and its novel effects in the development of the nervous system, and the effect of endogenously produced and exogenously administered MLT in reducing the degree of tissue and nerve injuries. MLT was recently reported to be an effective free radical scavenger and antioxidant. Since endogenous MLT levels fall significantly in senility, these findings imply that the loss of this antioxidant could contribute to the incidence or severity of some age-related neurodegenerative diseases. Considering the high efficacy of MLT in overcoming much of the injury not only to the peripheral nerve but also to other organs, clinical trials for this purpose should be seriously considered.

Atrioventricular septal defect with tetralogy of Fallot

1991 ◽  
Vol 1 (4) ◽  
pp. 396-398
Author(s):  
Bharat Dalvi ◽  
Krishnagopal Gupta ◽  
Satyavan Sharma
Keyword(s):  
Tetralogy Of Fallot ◽  
Septal Defect ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Atrioventricular Septal Defect ◽  
Cross Sectional

SummaryWe present a case of atrioventricular septal defect associated with tetralogy of Fallot which was diagnosed by cross-sectional echocardiography and angiography. The diagnosis was confirmed at necropsy. This case is unusual for the absence of Down's syndrome. We discuss the role of clinical, echocardiographic, hemodynamic and angiographic studies.

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Microglial Cells ◽  
Inflammatory Reactions ◽  
Mental Diseases ◽  
The Central Nervous System ◽  
The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

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