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- Aldskogius, Håkan, et al.
(författare)
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Microglia and Neuropathic Pain
- 2013
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Ingår i: CNS & Neurological Disorders. - : Wiley. - 1871-5273 .- 1996-3181. ; 12:6, s. 768-772
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Tidskriftsartikel (refereegranskat)abstract
- Neuropathic pain is a serious consequence of injury or disease in the nervous system itself. Current treatment options for this condition are often unsatisfactory. From being originally viewed as a diseased caused by neuronal dysfunction, a growing body of evidence implicate activated microglia as a key player in the development of this pain condition. In this review, some of the evidence for this proposal is briefly discussed and placed in a translational context, pointing out the difficulties in translating commonly used animal models of neuropathic pain to the clinical condition, as well as emphasizing the broader role of activated microglia in the injured or diseased nervous system.
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| 2. |
- Archer, Trevor, 1949, et al.
(författare)
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Effects of physical exercise on depressive symptoms and biomarkers in depression
- 2014
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Ingår i: CNS & Neurological Disorders. - Bussum : Bentham Science Publishers. - 1871-5273 .- 1996-3181. ; 13:10, s. 1640-1653
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Tidskriftsartikel (refereegranskat)abstract
- Regular physical exercise/activity has been shown repeatedly to promote positive benefits in cognitive, emotional and motor domains concomitant with reductions in distress and negative affect. It exerts a preventative role in anxiety and depressive states and facilitates psychological well-being in both adolescents and adults. Not least, several meta-analyses attest to improvements brought about by exercise. In the present treatise, the beneficial effects of exercise upon cognitive, executive function and working memory, emotional, self-esteem and depressed mood, motivational, anhedonia and psychomotor retardation, and somatic/physical, sleep disturbances and chronic aches and pains, categories of depression are discussed. Concurrently, the amelioration of several biomarkers associated with depressive states: hypothalamic-pituitary-adrenal (HPA) axis homeostasis, anti-neurodegenerative effects, monoamine metabolism regulation and neuroimmune functioning. The notion that physical exercise may function as "scaffolding" that buttresses available network circuits, anti-inflammatory defences and neuroreparative processes, e.g. brain-derived neurotrophic factor (BDNF), holds a certain appeal. © 2014 Bentham Science Publishers.
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| 5. |
- Cipriano, Mariateresa, et al.
(författare)
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Palmitoylethanolamide regulates production of pro-angiogenic mediators in a model of β amyloid-induced astrogliosis in vitro
- 2015
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Ingår i: CNS & Neurological Disorders. - : Bentham Science Publishers B.V.. - 1871-5273 .- 1996-3181. ; 14:7, s. 828-837
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Tidskriftsartikel (refereegranskat)abstract
- Aβ-induced astrogliosis can worsen the eziopathogenesis of Alzheimer disease (AD) by the release of proinflammatory and pro-oxidant mediators. Activated glial cells may release also pro-angiogenic molecules. The role of angiogenesis in AD is still controversial: although angiogenesis brings oxygen and nutrients to injured tissue, it may also exacerbate reactive gliosis. Moreover, by altering blood-brain barrier permeability pro-angiogenic mediators promote passage of inflammatory/immune-competent cells into the brain, thereby exacerbating gliosis. The release of proangiogenic factors during astrogliosis may thus be a key-step in controlling AD progression. The endogenous fatty acid amide, palmitoylethanolamide (PEA), is a pleiotropic mediator exerting anti-inflammatory, antinociceptive and antiangiogenic effects in several in vitro and in vivo models of chronic-degenerative disease. In this study, we investigated the effects of PEA in AD angiogenesis and neuroinflammation by using conditioned medium from untreated and Aβ-treated C6 rat astroglioma cells and HUVEC human endothelial cells. PEA (10-8-10-6 M) concentration-dependently reduced expression of pro-inflammatory and pro-angiogenic markers in Aβ (1 μg/mL)-stimulated C6 cells. Moreover, culture medium from PEA-treated C6 cells reduced HUVEC cell proliferation as compared to cells treated with conditioned medium from Aβ-treated C6 cells. Immunocytochemical analysis revealed that PEA treatment inhibited nuclear levels of mitogen-activated protein kinase 1 (the main pro-angiogenic pathway) and cytoplasmic vascular endothelial growth factor in HUVEC cells receiving C6 conditioned medium. Finally, the peroxisome proliferator-activated receptor alpha inhibitor GW6471, added to Aβ-treated C6 cells blocked all PEA effects in this model, suggesting that PEA acts through a proliferator-activated receptor alpha-dependent mechanism on astroglial cells. Collectively, these data support the potential therapeutic utility of PEA in AD.
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| 8. |
- Huang, Hongyun, et al.
(författare)
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Neurorestoratology : New Advances in Clinical Therapy
- 2023
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Ingår i: CNS & Neurological Disorders. - : Bentham Science Publishers. - 1871-5273 .- 1996-3181. ; 22:7, s. 1031-1038
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Forskningsöversikt (refereegranskat)abstract
- Neurorestorative treatments have been able to improve the quality of life for patients suffering from neurological diseases and damages since the concept of Neurorestoratology was proposed. The discipline of Neurorestoratology focuses on restoring impaired neurological functions and/or structures through varying neurorestorative mechanisms including neurostimulation or neuromodulation, neuroprotection, neuroplasticity, neuroreplacement, loop reconstruction, remyelination, immunoregulation, angiogenesis or revascularization, neuroregeneration or neurogenesis and others. The neurorestorative strategies of Neurorestoratology include all therapeutic methods which can restore dysfunctions for patients with neurological diseases and improve their quality of life. Neurorestoratology is different from regenerative medicine in the nervous system, which mainly focuses on the neuroregeneration. It also is different from Neurorehabilitation. Neurorestoratology and Neurorehabilitation share some functional recovering mechanisms, such as neuroplasticity, especially in the early phase of neurological diseases; but generally Neurorehabilitation mainly focuses on recovering neurological functions through making the best use of residual neurological functions, replacing lost neurological functions in the largest degree, and preventing and treating varying complications. Recently, there have been more advances in restoring damaged nerves by cell therapy, neurostimulation/neuromodulation and brain-computer interface (BCI), neurorestorative surgery, neurorestorative pharmaceutics, and other clinic strategies. Simultaneously related therapeutic guidelines and standards are set up in succession. Based on those advances, clinicians should consider injured and degenerated nervous disorders or diseases in the central nervous system as treatable or neurorestorative disorders. Extending and encouraging further neurorestorative explorations and achieving better clinical efficacy with stronger evidence regarding neurorestoratology will shed new light and discover superior benefits for patients with neurological disorders.
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| 9. |
- Kiyatkin, Eugene A., et al.
(författare)
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Breakdown of Blood-Brain and Blood-Spinal Cord Barriers During Acute Methamphetamine Intoxication : Role of Brain Temperature
- 2016
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Ingår i: CNS & Neurological Disorders. - : Bentham Science Publishers Ltd.. - 1871-5273 .- 1996-3181. ; 15:9, s. 1129-1138
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Forskningsöversikt (refereegranskat)abstract
- Methamphetamine (METH) is a powerful and often-abused stimulant with potent addictive and neurotoxic properties. While it is generally believed that structural brain damage induced by METH results from oxidative stress, in this work we present data suggesting robust disruption of blood-brain and blood-spinal cord barriers during acute METH intoxication in rats. We demonstrate the relationships between METH-induced brain hyperthermia and widespread but structure-specific barrier leakage, acute glial cell activation, changes in brain water and ionic homeostasis, and structural damage of different types of cells in the brain and spinal cord. Therefore, METH-induced leakage of the blood-brain and blood-spinal cord barriers is a significant contributor to different types of functional and structural brain abnormalities that determine acute toxicity of this drug and possibly neurotoxicity during its chronic use.
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| 10. |
- Kiyatkin, Eugene A., et al.
(författare)
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Not Just the Brain : Methamphetamine Disrupts Blood-Spinal Cord Barrier and Induces Acute Glial Activation and Structural Damage of Spinal Cord Cells
- 2015
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Ingår i: CNS & Neurological Disorders. - 1871-5273 .- 1996-3181. ; 14:2, s. 282-294
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Tidskriftsartikel (refereegranskat)abstract
- Acute methamphetamine (METH) intoxication induces metabolic brain activation as well as multiple physiological and behavioral responses that could result in life-threatening health complications. Previously, we showed that METH (9 mg/kg) used in freely moving rats induces robust leakage of blood-brain barrier, acute glial activation, vasogenic edema, and structural abnormalities of brain cells. These changes were tightly correlated with drug-induced brain hyperthermia and were greatly potentiated when METH was used at warm ambient temperatures (29 degrees C), inducing more robust and prolonged hyperthermia. Extending this line of research, here we show that METH also strongly increases the permeability of the blood-spinal cord barrier as evidenced by entry of Evans blue and albumin immunoreactivity in T9-12 segments of the spinal cord. Similar to the blood-brain barrier, leakage of bloodspinal cord barrier was associated with acute glial activation, alterations of ionic homeostasis, water tissue accumulation (edema), and structural abnormalities of spinal cord cells. Similar to that in the brain, all neurochemical alterations correlated tightly with drug-induced elevations in brain temperature and they were enhanced when the drug was used at 29 degrees C and brain hyperthermia reached pathological levels (>40 degrees C). We discuss common features and differences in neural responses between the brain and spinal cord, two inseparable parts of the central nervous system affected by METH exposure.
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