| 1. |
- Kiyatkin, Eugene A., et al.
(författare)
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Acute Methamphetamine Intoxication : Brain Hyperthermia, Blood–Brain Barrier, Brain Edema, and morphological cell abnormalities
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 65-100
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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 assumed that multiple chemical substances released in the brain following METH-induced metabolic activation (or oxidative stress) are primary factors underlying damage of neural cells, in this work we present data suggesting a role of brain hyperthermia and associated leakage of the blood-brain barrier (BBB) in acute METH-induced toxicity. First, we show that METH induces a dose-dependent brain and body hyperthermia, which is strongly potentiated by associated physiological activation and in warm environments that prevent proper heat dissipation to the external environment. Second, we demonstrate that acute METH intoxication induces robust, widespread but structure-specific leakage of the BBB, acute glial activation, and increased water content (edema), which are related to drug-induced brain hyperthermia. Third, we document widespread morphological abnormalities of brain cells, including neurons, glia, epithelial, and endothelial cells developing rapidly during acute METH intoxication. These structural abnormalities are tightly related to the extent of brain hyperthermia, leakage of the BBB, and brain edema. While it is unclear whether these rapidly developed morphological abnormalities are reversible, this study demonstrates that METH induces multiple functional and structural perturbations in the brain, determining its acute toxicity and possibly contributing to neurotoxicity.
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| 2. |
- Landgraf, M., et al.
(författare)
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Development and Structure of Motoneurons
- 2006
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 75, s. 33-53
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Forskningsöversikt (refereegranskat)
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| 3. |
- Nyberg, Fred, 1945-
(författare)
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The role of the somatotrophic axis in neuroprotection and neuroregeneration of the addictive brain
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 399-427
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Forskningsöversikt (refereegranskat)abstract
- Early studies have shown that the abuse of alcohol, central stimulants, and opiates such as heroin destroys brain cells, reducing attention span and memory. However, new research has suggested that there may be a way to regain some of the lost attention and recall. It has recently been shown that brain cells targeted for early death by continued opiate use can be salvaged by injections of synthetic human growth hormone (GH). GH is a polypeptide hormone, normally secreted by the anterior pituitary gland, which stimulates cell growth and controls body metabolism. Recombinant human GH is currently used in replacement therapy to alleviate the symptoms of adults and children with GH deficiency syndrome. The recent observation that GH can reverse morphine-induced cell damage could open the door to new ways of treating and preventing damage from the abuse of opiates in addicts and also of treating cell damage induced by alcohol and central stimulants. This article reviews current knowledge of the somatotrophic axis, including GH and insulin-like growth factor-1 (IGF-1), in the brain and also discusses the potential use of GH/IGF-1 as agents for treatment of brain pathology in addictive diseases.
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| 4. |
- Sharma, Hari Shanker, et al.
(författare)
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Cocaine-Induced Breakdown of the Blood–Brain Barrier and Neurotoxicity
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 297-334
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Forskningsöversikt (refereegranskat)abstract
- Role of cocaine in influencing blood-brain barrier (BBB) function is still unknown. Available evidences suggest that cocaine administration results in acute hyperthermia and alterations in brain serotonin metabolism. Since hyperthermia is capable to induce the breakdown of the BBB either directly or through altered serotonin metabolism, a possibility exists that cocaine may induce neurotoxicity by causing BBB disruption. This hypothesis is discussed in this review largely based on our own laboratory investigations. Our observations in rats demonstrate that cocaine depending on the dose and routes of administration induces profound hyperthermia, increased plasma and brain serotonin levels leading to BBB breakdown and brain edema formation. Furthermore, cocaine was able to enhance cellular stress as seen by upregulation of heat shock protein (HSP 72 kD) expression and resulted in marked neuronal and glial cell damages at the time of the BBB dysfunction. Taken together, these observations are the first to suggest that cocaine-induced BBB disruption is instrumental in precipitating brain pathology. The possible mechanisms of cocaine-induced BBB breakdown and neurotoxicity are discussed.
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| 5. |
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| 6. |
- Terenghi, Giorgio, et al.
(författare)
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Chapter 21 : Use of stem cells for improving nerve regeneration
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 87, s. 393-403
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Forskningsöversikt (refereegranskat)abstract
- A clear need exists for new surgical approaches to enhance the recuperation of functions after peripheral nerve injury and repair. At present, advances in the regenerative medicine fields of biomaterials, cellular engineering, and molecular biology are all contributing to the development of a bioengineered nerve implant, which could be used clinically as an alternative to nerve autograft. In this review we examine the recent progress in this field, looking in particular at the applicability of Schwann cells and stem cell transplantation to enhance nerve regeneration.
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| 7. |
- Cedergren Weber, Gustav, et al.
(författare)
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Diagnostic work up : Laboratory and biomarkers
- 2022
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Ingår i: International Review of Neurobiology. - : Elsevier. - 0074-7742 .- 2162-5514. ; 162, s. 53-96
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Bokkapitel (refereegranskat)abstract
- This chapter will focus on the diagnostic work around sexual dysfunction in Parkinson's disease, especially laboratory tests and biomarkers. A number of methods to analyze if sexual dysfunction is caused by neural pathology, vascular dysfunction or other mechanisms are now available. Other methods can be used to differentiate between psychogenic/functional reasons behind sexual dysfunction and organic ones. The role of biomarkers for diagnosis, but also for understanding the reason behind and for counteracting sexual dysfunction is becoming more evident. There is also a rich and increasing number of scales and other instruments available for detecting and quantifying sexual hypo- and hyperactivity. When investigating the reason behind sexual dysfunction in patients with Parkinson's disease comorbidities should also be considered. Finally, early and pronounced sexual dysfunction might in some cases be an indication that differential diagnosis, like Multisystem Atrophy, should be thought about. All these aspects of the diagnostic procedures around sexual dysfunction in Parkinson's disease will be covered in this chapter.
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| 8. |
- Gaab, Jens, et al.
(författare)
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Placebo and psychotherapy : differences, similarities, and implications
- 2018
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Ingår i: International review of neurobiology. - : Elsevier. - 0074-7742 .- 2162-5514. ; 138, s. 241-255
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Forskningsöversikt (refereegranskat)abstract
- The placebo and psychotherapy are both effective psychological interventions. Next to being characterized by their own and specific controversies and debates, there is a persistent-and least for psychotherapy-looming notion that these two interventions share more than just the first letter. Based on Grunbaum's influential conceptualization of placebo, this chapter critically reviews both the time-honored claim that psychotherapy is a placebo as well as the argument that the placebo concept does not translate to psychotherapy. We conclude that there is an unwanted proximity between these two interventions and that empirical attempts to separate the "wheat from the chaff" in psychotherapy research face several distinctive challenges and thus are often methodologically comprised by the integrity of the placebo. However, drawing on recent, innovative research, we conclude that psychotherapy can be saved, i.e., shown to be distinct from the placebo, by employing study designs derived from the placebo research. We conclude that the placebo concept has profound implications for psychotherapy, psychotherapy research, and last but not least its ethical practice.
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| 9. |
- Pantazis, Antonios, et al.
(författare)
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Biophysics of BK Channel Gating
- 2016
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Ingår i: International review of neurobiology. - : Elsevier. - 0074-7742 .- 2162-5514. ; 128, s. 1-49
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Forskningsöversikt (refereegranskat)abstract
- BK channels are universal regulators of cell excitability, given their exceptional unitary conductance selective for K(+), joint activation mechanism by membrane depolarization and intracellular [Ca(2+)] elevation, and broad expression pattern. In this chapter, we discuss the structural basis and operational principles of their activation, or gating, by membrane potential and calcium. We also discuss how the two activation mechanisms interact to culminate in channel opening. As members of the voltage-gated potassium channel superfamily, BK channels are discussed in the context of archetypal family members, in terms of similarities that help us understand their function, but also seminal structural and biophysical differences that confer unique functional properties.
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| 10. |
- Sharma, Hari Shanker, et al.
(författare)
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Neuroprotective effects of cerebrolysin, a combination of different active fragments of neurotrophic factors and peptides on the whole body hyperthermia-induced neurotoxicity : modulatory roles of co-morbidity factors and nanoparticle intoxication
- 2012
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 102, s. 249-276
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Tidskriftsartikel (refereegranskat)abstract
- Military personals are often exposed to adverse environmental circumstances, for example, heat stress during peacekeeping or combat operations in summer months or in desert areas leading to disturbed mental functions. The suitable therapeutic strategies to treat heat-induced mental anomalies are still not worked out. Thus, exploration of suitable therapeutic strategies to minimize heat-induced abnormal brain function is needed in suitable animal models. Previous works from our laboratory show that rats exposed to whole body hyperthermia (WBH) for 4 h at 38 °C exhibited profound neuronal, glial, and axonal damages in the cerebral cortex, hippocampus, cerebellum, thalamus, and hypothalamus in a specific manner at light microscopy. Electron microscopy further revealed endothelial cell membrane damage, that is, breakdown of the blood-brain barrier (BBB) after WBH in the brain areas showing cellular damages. These observations indicate that breakdown of the BBB is instrumental in hyperthermia-induced brain injury. Pretreatment with cerebrolysin (2.5 ml or 5 ml/kg, i.v. 30 min before WBH), a mixture of various neurotropic factors and active peptide fragments significantly attenuated BBB disruption and brain damage following heat exposure in a dose-dependent manner. Furthermore, repeated administration of cerebrolysin (5 ml/kg, i.v.) starting from 30 min to 1h after but not after 1.5 or 2 h WBH markedly reduced the BBB disruption and neurotoxicity. Taken together our observations suggest that cerebrolysin if administered within 1 h after WBH in suitable doses induce marked reduction in neurotoxicity. This indicated that cerebrolysin has potential therapeutic value to treat heat stress victims to prevent mental dysfunction in future clinical settings.
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