scholarly journals Role of PPARγin the Differentiation and Function of Neurons

PPAR Research ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Rodrigo A. Quintanilla ◽  
Elias Utreras ◽  
Fabián A. Cabezas-Opazo
Keyword(s):  
Neuropathic Pain ◽  
Neurodegenerative Disorders ◽  
Neuronal Death ◽  
Neuronal Development ◽  
Brain Cells ◽  
Neuronal Processes ◽  
And Function ◽  
Pain Regulation ◽  
Important Evidence

Neuronal processes (neurites and axons) have an important role in brain cells communication and, generally, they are damaged in neurodegenerative diseases. Recent evidence has showed that the activation of PPARγpathway promoted neuronal differentiation and axon polarity. In addition, activation of PPARγusing thiazolidinediones (TZDs) prevented neurodegeneration by reducing neuronal death, improving mitochondrial function, and decreasing neuroinflammation in neuropathic pain. In this review, we will discuss important evidence that supports a possible role of PPARγin neuronal development, improvement of neuronal health, and pain signaling. Therefore, activation of PPARγis a potential target with therapeutic applications against neurodegenerative disorders, brain injury, and pain regulation.

Neurodegenerative disorders in older people

2020 ◽  
pp. 601-611
Author(s):  
John Hindle
Keyword(s):  
Risk Factors ◽  
Older People ◽  
Protective Factors ◽  
Genetic Susceptibility ◽  
Neurodegenerative Disorders ◽  
Neuronal Death ◽  
Clinical Signs ◽  
Symptomatic Treatment ◽  
Structure And Function ◽  
And Function

Neurodegenerative disorders are associated with a progressive loss of structure and function of neurones that leads to neuronal death. Their aetiology combines ageing, genetic susceptibility, and risk factors including environmental exposure, balanced against protective factors. They present with varying combinations of progressive cognitive, emotional, motor, autonomic and peripheral symptoms, and clinical signs. Neurodegenerative conditions are all likely to have a preclinical prodromal period, followed by slow initial decline during which there is clinical presentation, followed by a further steady decline and an eventual accelerated decline. The rate of progression of these disorders varies greatly, but they are all inevitably progressive, currently have no cure, and require symptomatic treatment.

scholarly journals MiR-9 and the Midbrain-Hindbrain Boundary: A Showcase for the Limited Functional Conservation and Regulatory Complexity of MicroRNAs

2020 ◽  
Vol 8 ◽  
Author(s):  
A. Alwin Prem Anand ◽  
Gonzalo Alvarez-Bolado ◽  
Andrea Wizenmann
Keyword(s):  
Neuronal Development ◽  
Brain Size ◽  
Regulatory System ◽  
Large Degree ◽  
Regulate Gene Expression ◽  
Functional Conservation ◽  
Regulatory Complexity ◽  
Species Specific ◽  
And Function

MicroRNAs regulate gene expression at post-transcriptional levels. Some of them appear to regulate brain development and are involved in neurodevelopmental disorders. This has led to the suggestion that the role of microRNAs in neuronal development and function may be more central than previously appreciated. Here, we review the data about miR-9 function to depict the subtlety, complexity, flexibility and limited functional conservation of this essential developmental regulatory system. On this basis we propose that species-specific actions of miR-9 could underlie to a large degree species differences in brain size, shape and function.

Neurochemistry

2017 ◽  
pp. 167-206
Author(s):  
Eduardo E. Benarroch ◽  
Jeremy K. Cutsforth-Gregory ◽  
Kelly D. Flemming
Keyword(s):  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Neuronal Death ◽  
Synaptic Cleft ◽  
Pharmacologic Treatment ◽  
Neurotransmitter Systems ◽  
Neuronal Excitation ◽  
Chemical Synapses ◽  
And Function ◽  
Excitability Of Neurons

Communication between neurons occurs primarily at the level of synapses. The most common form of communication in the nervous system is through chemical synapses, which consist of presynaptic and postsynaptic components separated by a synaptic cleft. The presynaptic terminals contain synaptic vesicles, which are involved in the storage and release of neurotransmitters by the process of exocytosis. Complex mechanisms control the synthesis, vesicular storage, and release of neurotransmitters and regulate the availability of neurotransmitter at the level of the synaptic cleft. The effects of the neurochemical transmitter on its target are mediated by neurotransmitter receptors. Specific neurotransmitter systems are responsible for fast neuronal excitation or inhibition, while other neurotransmitter systems regulate the excitability of neurons in the nervous system. Abnormalities in neurochemical transmission are responsible for many disorders, including acute neuronal death, seizures, neurodegenerative disorders, and psychiatric diseases. Most importantly, neurochemical systems provide the target for pharmacologic treatment of these disorders. The aims of this chapter are to review the basis of neurochemical transmission and the distribution, biochemistry, and function of specific neurotransmitter systems.

scholarly journals The role of connexin43 in neuropathic pain induced by spinal cord injury

2019 ◽  
Vol 51 (6) ◽  
pp. 555-561 ◽  
Author(s):  
Anhui Wang ◽  
Changshui Xu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Cell Metabolism ◽  
Pain Models ◽  
Cord Injury ◽  
The Central Nervous System ◽  
And Function

Abstract Neuropathic pain is caused by the damage or dysfunction of the nervous system. In many neuropathic pain models, there is an increase in the number of gap junction (GJ) channels, especially the upregulation of the expression of connexin43 (Cx43), leading to the secretion of various types of cytokines and involvement in the formation of neuropathic pain. GJs are widely distributed in mammalian organs and tissues, and Cx43 is the most abundant connexin (Cx) in mammals. Astrocytes are the most abundant glial cell type in the central nervous system (CNS), which mainly express Cx43. More importantly, GJs play an important role in regulating cell metabolism, signaling, and function. Many existing literatures showed that Cx43 plays an important role in the nervous system, especially in the CNS under normal and pathological conditions. However, many internal mechanisms have not yet been thoroughly explored. In this review, we summarized the current understanding of the role and association of Cx and pannexin channels in neuropathic pain, especially after spinal cord injury, as well as some of our own insights and thoughts which suggest that Cx43 may become an emerging therapeutic target for future neuropathic pain, bringing new hope to patients.

scholarly journals Microtubules are necessary for proper Reticulon localization during mitosis

2019 ◽  
Author(s):  
Zane J. Bergman ◽  
Ulises Diaz ◽  
Amanda Sims ◽  
Blake Riggs
Keyword(s):  
Endoplasmic Reticulum ◽  
Neurodegenerative Disorders ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Microtubule Cytoskeleton ◽  
Spindle Poles ◽  
And Function ◽  
Insight Into

AbstractDuring mitosis, the structure of the Endoplasmic Reticulum (ER) displays a dramatic reorganization and remodeling event, however the mechanism driving these changes is poorly understood. Recently, the Reticulon family of ER shaping proteins has been identified as possible factors to promote these drastic changes in ER morphology. In addition, the Reticulons and other ER shaping proteins have been directly linked to several hereditary neurodegenerative disorders. Here, we provide key insight into the cytoskeletal factors involved in the Drosophila Reticulon, Reticulon-like 1 (Rtnl1) during mitosis in the early embryo. At prometaphase, Rtnl1 localizes at the spindle poles just prior to the bulk of ER localization suggesting a role in recruitment. Using precise temporal injections of cytoskeletal inhibitors in the early syncytial Drosophila embryo, we show that microtubules, not microfilaments are necessary for proper Rtnl1 localization and function during mitosis. Lastly, we show that astral microtubules are necessary for Rtnl1 localization at the spindle poles early in mitosis. This work highlights the role of the microtubule cytoskeleton in Rtnl1 localization and ER dynamics during mitosis and sheds light on a pathway towards inheritance of this major organelle.

scholarly journals Nrf2 activation in the treatment of neurodegenerative diseases: a focus on its role in mitochondrial bioenergetics and function

2016 ◽  
Vol 397 (5) ◽  
pp. 383-400 ◽  
Author(s):  
Noemí Esteras ◽  
Albena T. Dinkova-Kostova ◽  
Andrey Y. Abramov
Keyword(s):  
Transcription Factor ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Related Factor ◽  
Mitochondrial Bioenergetics ◽  
Cytoprotective Activity ◽  
Nrf2 Activation ◽  
Potential Therapeutic Role ◽  
And Function

Abstract The nuclear factor erythroid-derived 2 (NF-E2)-related factor 2 (Nrf2) is a transcription factor well-known for its function in controlling the basal and inducible expression of a variety of antioxidant and detoxifying enzymes. As part of its cytoprotective activity, increasing evidence supports its role in metabolism and mitochondrial bioenergetics and function. Neurodegenerative diseases are excellent candidates for Nrf2-targeted treatments. Most neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and Friedreich’s ataxia are characterized by oxidative stress, misfolded protein aggregates, and chronic inflammation, the common targets of Nrf2 therapeutic strategies. Together with them, mitochondrial dysfunction is implicated in the pathogenesis of most neurodegenerative disorders. The recently recognized ability of Nrf2 to regulate intermediary metabolism and mitochondrial function makes Nrf2 activation an attractive and comprehensive strategy for the treatment of neurodegenerative disorders. This review aims to focus on the potential therapeutic role of Nrf2 activation in neurodegeneration, with special emphasis on mitochondrial bioenergetics and function, metabolism and the role of transporters, all of which collectively contribute to the cytoprotective activity of this transcription factor.

scholarly journals The Effects of Leptin Replacement on Neural Plasticity

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Gilberto J. Paz-Filho
Keyword(s):  
Neural Plasticity ◽  
Observational Studies ◽  
Neuronal Development ◽  
Neuronal Morphology ◽  
Synaptic Activity ◽  
Hypothalamic Amenorrhea ◽  
Glutamate Receptor Trafficking ◽  
Brain Structure And Function ◽  
And Function

Leptin, an adipokine synthesized and secreted mainly by the adipose tissue, has multiple effects on the regulation of food intake, energy expenditure, and metabolism. Its recently-approved analogue, metreleptin, has been evaluated in clinical trials for the treatment of patients with leptin deficiency due to mutations in the leptin gene, lipodystrophy syndromes, and hypothalamic amenorrhea. In such patients, leptin replacement therapy has led to changes in brain structure and function in intra- and extrahypothalamic areas, including the hippocampus. Furthermore, in one of those patients, improvements in neurocognitive development have been observed. In addition to this evidence linking leptin to neural plasticity and function, observational studies evaluating leptin-sufficient humans have also demonstrated direct correlation between blood leptin levels and brain volume and inverse associations between circulating leptin and risk for the development of dementia. This review summarizes the evidence in the literature on the role of leptin in neural plasticity (in leptin-deficient and in leptin-sufficient individuals) and its effects on synaptic activity, glutamate receptor trafficking, neuronal morphology, neuronal development and survival, and microglial function.

Sign in / Sign up

Export Citation Format

Share Document