| 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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| 11. |
- Wasén, Caroline, 1990, et al.
(författare)
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The emerging role of the microbiome in Alzheimer's disease
- 2022
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Ingår i: International Review of Neurobiology. - : Elsevier. - 2162-5514 .- 0074-7742.
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Alzheimer's disease (AD) is the most prevalent form of dementia and can be influenced by genetic and environmental factors. Recent studies suggest that the intestinal microbiota is altered in AD patients when compared to healthy individuals and may play a role in disease onset and progression. Aging is the greatest risk factor for AD, and age-related changes in the microbiota can affect processes that contribute to cognitive decline. The microbiota may affect AD by modulating peripheral and central immunity or by secreting factors that influence neurogenesis or neuronal cell death. Finally, probiotic and dietary interventions that target the microbiome may have therapeutic potential to prevent or treat AD.
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| 12. |
- Bontioti, Eleana, et al.
(författare)
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Mechanisms underlying the end-to-side nerve regeneration
- 2009
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Ingår i: International Review of Neurobiology. - 0074-7742. ; 87, s. 251-268
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Forskningsöversikt (refereegranskat)abstract
- End-to-side (ETS) nerve repair is used in selected clinical cases. The mechanisms, by which regeneration into the attached nerve segment is initiated and occur, are still not fully understood. Based on numerous experimental studies, different mechanisms have been Suggested by which regenerating axons are recruited, such as contamination From the proximal nerve segment, collateral sprouting, and terminal regenerating sprouting from the donor nerve. A variety of experimental models, most commonly in the lower and upper extremity of rats, and techniques have been used to shed light on the mechanisms. Retrograde labeling techniques have revealed that collateral sprouting do occur, but is probably, at least as observed in long-term experiments, less important over time. Pruning of branching nerve fibers, induced by the collateral sprouting, is an additional mechanism in this context. Experiments have also focused on the stimuli, including the question of epineurial or perineurial windows, that trigger the sprouting of axons form the donor nerve, which can detected by the use of markers of cellular injury. In die present article, we review studies contributing to clarifications of mechanisms of end-to-side nerve repair, including used experimental techniques. We also stress the importance of the plastic brain.
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| 13. |
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| 14. |
- Jakobsson, Johan, et al.
(författare)
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Lentiviral vectors.
- 2003
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Ingår i: International Review of Neurobiology. - 0074-7742. ; 55, s. 111-122
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Forskningsöversikt (refereegranskat)
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| 15. |
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| 16. |
- Fredholm, BB, et al.
(författare)
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Adenosine and brain function
- 2005
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Ingår i: International review of neurobiology. - 0074-7742. ; 63, s. 191-270
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Tidskriftsartikel (refereegranskat)
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| 17. |
- Pekny, Milos, 1965, et al.
(författare)
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The role of astrocytes and complement system in neural plasticity.
- 2007
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Ingår i: International review of neurobiology. - 0074-7742. ; 82, s. 95-111
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Forskningsöversikt (refereegranskat)abstract
- In neurotrauma, brain ischemia or neurodegenerative diseases, astrocytes become reactive (which is known as reactive gliosis) and this is accompanied by an altered expression of many genes. Two cellular hallmarks of reactive gliosis are hypertrophy of astrocyte processes and the upregulation of the part of the cytoskeleton known as intermediate filaments, which are composed of nestin, vimentin, and GFAP. Our aim has been to better understand the function of reactive astrocytes in CNS diseases. Using mice deficient for astrocyte intermediate filaments (GFAP(-/-)Vim(-/-)), we were able to attenuate reactive gliosis and slow down the healing process after neurotrauma. We demonstrated the key role of reactive astrocytes in neurotrauma-at an early stage after neurotrauma, reactive astrocytes have a neuroprotective effect; at a later stage, they facilitate the formation of posttraumatic glial scars and inhibit CNS regeneration, specifically, they seem to compromise neural graft survival and integration, reduce the extent of synaptic regeneration, inhibit neurogenesis in the old age, and inhibit regeneration of severed CNS axons. We propose that reactive astrocytes are the future target for the therapeutic strategies promoting regeneration and plasticity in the brain and spinal cord in various disease conditions. Through its involvement in inflammation, opsonization, and cytolysis, complement protects against infectious agents. Although most of the complement proteins are synthesized in CNS, the role of the complement system in the normal or ischemic CNS remains unclear. Complement activiation in the CNS has been generally considered as contributing to tissue damage. However, growing body of evidence suggests that complement may be a physiological neuroprotective mechanism as well as it may participate in maintenance and repair of the adult brain.
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| 18. |
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| 19. |
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| 20. |
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| 21. |
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| 22. |
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| 23. |
- Dahlin, Lars
(författare)
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The role of timing in nerve reconstruction.
- 2013
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Ingår i: International Review of Neurobiology. - 0074-7742. ; 109, s. 151-164
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Forskningsöversikt (refereegranskat)abstract
- The surgeon, who treats nerve injuries, should have knowledge about how peripheral nerves react to trauma, particularly an understanding about the extensive pathophysiological alterations that occur both in the peripheral and in the central nervous system. A large number of factors influence the functional outcome, where the surgeon only can affect a few of them. In view of the new knowledge about the delicate intracellular signaling pathways that are rapidly initiated in neurons and in nonneuronal cells with the purpose to induce nerve regeneration, the timing of nerve repair and reconstruction after injury has gained more interest. It is crucial to understand and to utilize the inborn mechanisms for survival and regeneration of neurons and for activation, survival, and proliferation of the Schwann cells and other cells that are acting after a nerve injury. Thus, experimental and clinical data clearly point toward the advantage of early nerve repair and reconstruction of injuries. Following an appropriate diagnosis of a nerve injury, the nerve should be promptly repaired or reconstructed, and new rehabilitation strategies should early be initiated. Considering nerve transfers in the treatment arsenal can shorten the time of nerve reinnervation of muscle targets. Timing of nerve repair and reconstruction is crucial after nerve injury.
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| 24. |
- Ffytche, DH, et al.
(författare)
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Psychosis in Parkinson's Disease
- 2017
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Ingår i: International review of neurobiology. - : Elsevier. - 2162-5514. ; 133, s. 585-622
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Tidskriftsartikel (refereegranskat)
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| 25. |
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| 26. |
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| 27. |
- Fredholm, BB, et al.
(författare)
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Adenosine and neuroprotection
- 1997
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Ingår i: International review of neurobiology. - 0074-7742. ; 40, s. 259-280
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Tidskriftsartikel (refereegranskat)
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| 28. |
- Hadamitzky, M, et al.
(författare)
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Placebo Effects in the Immune System
- 2018
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Ingår i: International review of neurobiology. - : Elsevier. - 2162-5514. ; 138, s. 39-59
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Tidskriftsartikel (refereegranskat)
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| 29. |
- Heurling, Kerstin, et al.
(författare)
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Disturbances in brain energy metabolism in insulin resistance and diabetes and Alzheimer's disease — Learnings from brain imaging biomarkers
- 2020
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Ingår i: International Review of Neurobiology. - : Elsevier. - 0074-7742. ; 154, s. 111-130
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Forskningsöversikt (refereegranskat)abstract
- Medical imaging techniques, such as structural and functional magnetic resonance imaging and positron emission tomography, have been used to gain a better understanding of the alterations of the metabolic processes in the brain relating to type 2 diabetes melltius, insulin resistance and Alzheimer's disease. These studies have shown that there are several similarities in the effects that these seemingly disparate diseases have on the brain, and that some of the abnormalities are reversed by metabolic interventions. This review provides an overview of the overlap between these diseases using medical imaging, focusing on glucose metabolism, mitochondrial function and lipid metabolism.
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| 30. |
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| 31. |
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| 32. |
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| 33. |
- Luchsinger, J. A., et al.
(författare)
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Tracking the potential involvement of metabolic disease in Alzheimer's disease—Biomarkers and beyond
- 2020
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Ingår i: International Review of Neurobiology. Vol. 154. - : Elsevier. - 0074-7742. - 9780128200766 ; , s. 51-77
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- There is a vast literature linking systemic metabolic conditions to dementia due to Alzheimer's disease (AD). Advances in in vivo measurements of AD neuropathology using brain imaging, cerebrospinal fluid (CSF), and/or blood biomarkers have led to research in AD that uses in vivo biomarkers as outcomes, focusing primarily on amyloid, tau, and neurodegeneration as constructs. Studies of Type 2 Diabetes Mellitus (T2DM) and AD biomarkers seem to show that T2DM is not related to amyloid deposition, but is related to neurodegeneration and tau deposition. There is a dearth of studies examining adiposity, insulin resistance, and metabolic syndrome in relation to AD biomarkers and the associations in these studies are inconsistent. Metabolomics studies have reported associations of unsaturated fatty acids with AD neuropathology at autopsy, and sphingolipids and glycerophospholipids in relation to neurodegeneration and amyloid and tau. There are other neurodegenerative diseases, such as Lewy body disease that may overlap with AD, and specific biomarkers for these pathologies are being developed and should be integrated into AD biomarker research. More longitudinal studies are needed with concurrent assessment of metabolic factors and AD biomarkers in order to improve the opportunity to assess causality. Ideally, AD biomarkers should be integrated into clinical trials of interventions that affect metabolic factors. Advances in blood-based AD biomarkers, which are less costly and invasive compared with CSF and brain imaging biomarkers, could facilitate widespread implementation of AD biomarkers in studies examining the metabolic contribution to AD. © 2020 Elsevier Inc.
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| 34. |
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| 35. |
- Mundt-Petersen, Ulrika, et al.
(författare)
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Infusional Therapies, Continuous Dopaminergic Stimulation, and Nonmotor Symptoms
- 2017
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Ingår i: Parkinson’s: The Hidden Face Management and the Hidden Face of Related Disorders. - : Elsevier. - 0074-7742. - 9780128126035 ; 134, s. 1019-1044
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Bokkapitel (refereegranskat)abstract
- Pump-based Parkinson (PD) therapies, including subcutaneous apomorphine infusion (CSA) and levodopa-carbidopa intestinal gel (LCIG), presently constitute the most effective pharmacological treatments available for advanced PD. These therapies are based on a more constant delivery of the dopaminergic drug resulting in a more continuous dopaminergic stimulation and a more stable treatment effect. This can be detected as reduction of time in off, reduction of dyskinesia frequency and severity, as well as increase of time in on without troublesome dyskinesias. A number of open-label studies now suggest that also the nonmotor PD symptomatology can improve under CSA and LCIG therapy. The most consistent improvements are seen concerning sleep, mood, and apathy, gastrointestinal symptoms, and urological symptoms. But also cardiovascular symptoms, perception, attention, and sexual function might show beneficial effects when moving from conventional therapies to pump treatment. Further there might be negative influences on some parts of the nonmotor symptomatology through side effects of CSA and LCIG therapy. In this chapter, we review the present knowledge about these aspects of the pump-based therapies. This information might be valuable when deciding on advanced therapy for individual patients.
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| 36. |
- Schank, Jesse R., et al.
(författare)
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Substance P and the Neurokinin-1 Receptor: The New CRF
- 2017
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Ingår i: ROLE OF NEUROPEPTIDES IN ADDICTION AND DISORDERS OF EXCESSIVE CONSUMPTION. - : ELSEVIER ACADEMIC PRESS INC. - 0074-7742. - 9780128124741 - 9780128124734 ; 136, s. 151-175
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Forskningsöversikt (refereegranskat)abstract
- Substance P (SP) is an 11-amino acid neuropeptide of the tachykinin family that preferentially activates the neurokinin-1 receptor (NK1R). First isolated 85 years ago and sequenced 40 years later, SP has been extensively studied. Early studies identified a role for SP and the NK1R in contraction of intestinal smooth muscle, central pain processing, and neurogenic inflammation. An FDA-approved NK1R antagonist, aprepitant, is used clinically for the treatment of chemotherapy-induced nausea, as the NK1R influences the activity of the brain stem emesis centers. More recently, SP and the NK1R have gained attention for their role in complex psychiatric processes including stress, anxiety, and depression. However, clinical development of NK1R antagonists for these indications has so far been unsuccessful. Several preclinical studies have also demonstrated a role of the NK1R in drug taking and drug seeking, especially as it relates to escalated consumption and stress-elicited seeking. This line of research developed in parallel with findings supporting a role of corticotropin-releasing factor (CRF) in stress-induced drug seeking. Over this time, CRF arguably gained more attention as a target for development of addiction pharmacotherapies. However, this effort has not resulted in a viable drug for use in human populations. Given promising clinical findings for the efficacy of NK1R antagonists on craving in alcoholics, along with recent data suggesting that a number of negative results from NK1R trials were likely due to insufficient receptor occupancy, the NK1R merits being revisited as a target for the development of novel pharmacotherapeutics for addiction.
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| 37. |
- Timpka, Jonathan, et al.
(författare)
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Device-Aided Treatment Strategies in Advanced Parkinson's Disease
- 2017
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Ingår i: International Review of Neurobiology. - : Elsevier. - 0074-7742. ; 132, s. 453-474
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Tidskriftsartikel (refereegranskat)abstract
- With peroral levodopa treatment, a majority of patients develop motor fluctuations and dyskinesia already within a few years of therapy. Device-aided Parkinson (PD) therapies refer to deep brain stimulation (DBS), levodopa-carbidopa intestinal gel infusion (LCIG), and subcutaneous infusion of the dopamine agonist apomorphine and represent effective strategies counteracting motor fluctuations and dyskinesia. These three therapy options seem to be similarly effective in reducing "time with PD symptoms (off time)" by at least 60%-65%. The use of advanced therapy also leads to a significant reduction of dyskinesia. Recent studies also indicate that these therapies can improve a number of nonmotor symptoms in advanced PD. Altogether this results in an improved health-related quality of life in most treated patients. The side effects and complications are quite different between the three; for DBS, serious adverse events include intracranial bleeding and infection, LCIG complications relate to the infusion equipment and the establishment of the percutaneous endoscopic gastrostomy, while for apomorphine infusion the most common side effect is a formation of noduli (local inflammation) at the point of infusion. The device-aided therapies are all indicated for the treatment of motor fluctuations and/or dyskinesia when peroral/transdermal PD medications cannot be further optimized. However, the choice of device-aided therapy is made on basis of indications/contraindications, but also the patients' symptom profile and his/her personal preferences. Therefore, it is important these treatments are discussed early, well before motor and nonmotor symptoms have deteriorated excessively.
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| 38. |
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