Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

Узбеков, М. Г.; Алферова, В. В.; Misionzhnik, E.; Гехт, А Б

doi:10.1007/s10517-011-1486-6

Cited by 3 publications

(3 citation statements)

References 8 publications

(14 reference statements)

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“…As such, studies have evaluated the isolation of these monoaminergic metabolites post-stroke and found increased concentrations in CSF using high-performance liquid chromatography (HPLC) (Tang et al, 1989; Wester et al, 1987). Additional work by Uzbekov et al (2011) analyzed blood samples from ischemic stroke patients and found increased MAO activity in stroke platelet samples several days after the initial ischemic insult. They suggested that this effect could be a compensatory mechanism to re-establish brain tissue homeostasis, as an increase in stroke monoamine activity is likely due to an increase in monoamine deamination activation and subsequent glutamate-induced excitotoxicity.…”

Section: Monoamine Neurotransmission Disruption Following Strokementioning

confidence: 99%

Executive (dys)function after stroke: special considerations for behavioral pharmacology

Povroznik¹,

Ozga

Haar

et al. 2018

Behavioural Pharmacology

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Stroke is a worldwide leading cause of death and long-term disability with concurrent secondary consequences that are largely comprised of mood dysfunction, as well as sensory, motor, and cognitive deficits. This review focuses on the cognitive deficits associated with stroke specific to executive dysfunction (including decision making, working memory, and cognitive flexibility) in humans, nonhuman primates, and additional animal models. Further, we review some of the cellular and molecular underpinnings of the individual components of executive dysfunction and their neuroanatomical substrates after stroke, with an emphasis on the changes that occur during biogenic monoamine neurotransmission. We concentrate primarily on changes in the catecholaminergic (dopaminergic and noradrenergic) and serotonergic systems at the levels of neurotransmitter synthesis, distribution, reuptake, and degradation. We also discuss potential secondary stroke-related behavioral deficits (specifically, poststroke depression as well as drug-abuse potential and addiction) and their relationship with stroke-induced deficits in executive function, an especially important consideration given that the average age of the human stroke population is decreasing. In the final sections, we address pharmacological considerations for the treatment of ischemia and the subsequent functional impairment, as well as current limitations in the field of stroke and executive function research.

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Section: Monoamine Neurotransmission Disruption Following Strokementioning

confidence: 99%

Executive (dys)function after stroke: special considerations for behavioral pharmacology

Povroznik¹,

Ozga

Haar

et al. 2018

Behavioural Pharmacology

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“…In rodents, MAO was reduced in the brain following 15-min ischemia, and the MAO activity never reached that of control levels during 7 days of reperfusion (Cvejic et al, 1980;Stanimirovic et al, 1994); In contrast, a different study showed that MAO was increased in the brain after a 22-h ischemia (Ansari et al, 2004). In clinical practice, during the acute period of ischemia stroke (3-5 days), MAO was increased in 25 patients compared to control levels, although the standard deviation was very high (Uzbekov et al, 2011). In our study, after 2-h ischemia, the MAO was decreased at 36 h, and salidroside (80 mg/kg) reversed the MAO levels.…”

Section: Discussionmentioning

confidence: 97%

“…In our study, after 2-h ischemia, the MAO was decreased at 36 h, and salidroside (80 mg/kg) reversed the MAO levels. A significant association between MAO activity and neurological deficits has been revealed by dynamic monitoring of patients with ischemia stroke, and the duration of ischemia is a key factor for stroke rehabilitation (Uzbekov et al, 2011;Crunkhorn, 2018). The effect of the dynamic variation of salidroside on MAO during different durations of ischemia is unclear and requires further studies.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

et al. 2019

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Salidroside, a phenylpropanoid glycoside, is the main bioactive component of Rhodiola rosea L. Salidroside has prominent anti-stroke effects in cerebral ischemia/reperfusion models. However, the underlying mechanisms of its actions are poorly understood. This study examined the anti-stroke effects of salidroside in middle cerebral artery occlusion (MCAO)-induced rat model of stroke and its potential mechanisms involving the dopaminergic system. Salidroside administration increased the levels of dopamine (DA), homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in the ipsilateral striatum after induction of transient ischemia, which were assessed using microdialysis with high-performance liquid chromatography coupled with electrochemical detection (HPLC-ECD). Furthermore, treatment with salidroside ameliorated neurobehavioral impairment, assessed with the modified neurological severity scores (mNSS), the balance beam test, and the foot fault test. Moreover, enzyme-linked immunosorbent assay (ELISA) suggested that MCAO-induced reduction in monoamine oxidase (MAO) was inhibited by salidroside. Immunohistochemical and immunofluorescence analyses revealed high level of tyrosine hydroxylase (TH) in the ipsilateral striatal caudate putamen (CPu) after cerebral ischemia/ reperfusion, which could be further elevated by salidroside. In addition, salidroside could reverse the decreased immunoreactivity of TH in the substantia nigra pars compacta (SNpc). These results suggest that the anti-stroke effects of salidroside in MCAO-induced cerebral ischemia/reperfusion may involve the modulation of monoamine metabolism in the striatum and SNpc, which may be related to the function of the dopaminergic system in the rat brain.

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Eryptosis as a marker of Parkinson's disease

Pretorius

Swanepoel

Buys

et al. 2014

Aging

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A major trend in recent Parkinson's disease (PD) research is the investigation of biological markers that could help in identifying at-risk individuals or to track disease progression and response to therapies. Central to this is the knowledge that inflammation is a known hallmark of PD and of many other degenerative diseases. In the current work, we focus on inflammatory signalling in PD, using a systems approach that allows us to look at the disease in a more holistic way. We discuss cyclooxygenases, prostaglandins, thromboxanes and also iron in PD. These particular signalling molecules are involved in PD pathophysiology, but are also very important in an aberrant coagulation/hematology system. We present and discuss a hypothesis regarding the possible interaction of these aberrant signalling molecules implicated in PD, and suggest that these molecules may affect the erythrocytes of PD patients. This would be observable as changes in the morphology of the RBCs and of PD patients relative to healthy controls. We then show that the RBCs of PD patients are indeed rather dramatically deranged in their morphology, exhibiting eryptosis (a kind of programmed cell death). This morphological indicator may have useful diagnostic and prognostic significance.

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Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

Cited by 3 publications

References 8 publications

Executive (dys)function after stroke: special considerations for behavioral pharmacology

Executive (dys)function after stroke: special considerations for behavioral pharmacology

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

Eryptosis as a marker of Parkinson's disease

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