Motor Cortex and Hippocampus Display Decreased Heme Oxygenase Activity 2 Weeks After Ventricular Fibrillation Cardiac Arrest in Rats

Warenits, Alexandra-Maria; Müllebner, Andrea; Ettl, Florian; Teubenbacher, Ursula; Magnet, Ingrid Anna Maria; Bauder, Barbara; Janata, Andreas; Miller, Ingrid; Moldzio, Rudolf; Kramer, Anne-Margarethe; Sterz, Fritz; Hölzer, Michael; Högler, Sandra; Weihs, Wolfgang; Duvigneau, Johanna Catharina

doi:10.3389/fmed.2020.00513

Cited by 3 publications

(2 citation statements)

References 75 publications

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“…Although all of our patients achieved relatively good neurological outcomes, some of the patients still suffered from mild motorial and sensorial symptoms. Warenits et al ( 35 ) found decreased neuronal function in the motor cortex, which is located in the precentral gyrus, and speculated it to be associated with motor deficits after CA in rats. Middleton et al ( 36 ) discovered diminished brain function in the somatosensory cortex in developing rats after CA.…”

Section: Discussionmentioning

confidence: 99%

A resting-state functional magnetic resonance imaging study of altered functional brain activity in cardiac arrest survivors with good neurological outcome

Wang

et al. 2023

Front. Neurol.

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PurposeTo investigate the spontaneous brain activity alterations in survivors of cardiac arrest (CA) with good neurological outcome using resting-state functional magnetic resonance imaging (rs-fMRI) with amplitude of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo) methods.Materials and methodsThirteen CA survivors with favorable neurological outcomes and 13 healthy controls (HCs) were recruited and underwent rs-fMRI scans. The ALFF and ReHo methods were applied to assess the regional intensity and synchronization of spontaneous brain activity. Correlation analyses were performed to explore the relationships between the mean ALFF and ReHo values in significant clusters and clinical parameters.ResultsThe survivors of CA showed significantly decreased ALFF values in the left postcentral gyrus and precentral gyrus and increased ALFF values in the left hippocampus and parahippocampal gyrus than HCs. Significantly decreased ReHo values were observed in the left inferior occipital gyrus and middle occipital gyrus in the patients. Mean ALFF values in the left hippocampus and parahippocampal gyrus were positively correlated with the time to return of spontaneous circulation (r = 0.794, p = 0.006) in the patient group.ConclusionFunctional activity alterations in the brain areas corresponding to known cognitive and physical impairments were observed in CA survivors with preserved neurological function. Our results could advance the understanding of the neurological mechanisms underlying the residual deficits in those patients.

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Section: Discussionmentioning

confidence: 99%

A resting-state functional magnetic resonance imaging study of altered functional brain activity in cardiac arrest survivors with good neurological outcome

Wang

et al. 2023

Front. Neurol.

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“…Transient global brain ischemia resulting from cardiac arrest in humans and animals causes neurodegeneration of neurons in the hippocampus, brain cortex, amygdala, basal ganglia, thalamus, dorsal and lateral septum, olfactory tubercle, primary olfactory cortex, entorhinal cortex, and brainstem [2,13,[30][31][32][33][34][35][36]. The hippocampus is one of the brain regions most susceptible to ischemia after cardiac arrest in humans [37][38][39] and in animals [40][41][42][43]. Transient global brain ischemia causes selective neurodegeneration in the CA1 area of the hippocampus in humans and animals within 2-7 days after reperfusion [30,42].…”

Section: Brain Neurodegeneration After Cardiac Arrestmentioning

confidence: 99%

Ischemia-Reperfusion Programming of Alzheimer’s Disease-Related Genes—A New Perspective on Brain Neurodegeneration after Cardiac Arrest

Pluta,

Czuczwar

2024

IJMS

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The article presents the latest data on pathological changes after cerebral ischemia caused by cardiac arrest. The data include amyloid accumulation, tau protein modification, neurodegenerative and cognitive changes, and gene and protein changes associated with Alzheimer’s disease. We present the latest data on the dysregulation of genes related to the metabolism of the amyloid protein precursor, tau protein, autophagy, mitophagy, apoptosis, and amyloid and tau protein transport genes. We report that neuronal death after cerebral ischemia due to cardiac arrest may be dependent and independent of caspase. Moreover, neuronal death dependent on amyloid and modified tau protein has been demonstrated. Finally, the results clearly indicate that changes in the expression of the presented genes play an important role in acute and secondary brain damage and the development of post-ischemic brain neurodegeneration with the Alzheimer’s disease phenotype. The data indicate that the above genes may be a potential therapeutic target for brain therapy after ischemia due to cardiac arrest. Overall, the studies show that the genes studied represent attractive targets for the development of new therapies to minimize ischemic brain injury and neurological dysfunction. Additionally, amyloid-related genes expression and tau protein gene modification after cerebral ischemia due to cardiac arrest are useful in identifying ischemic mechanisms associated with Alzheimer’s disease. Cardiac arrest illustrates the progressive, time- and area-specific development of neuropathology in the brain with the expression of genes responsible for the processing of amyloid protein precursor and the occurrence of tau protein and symptoms of dementia such as those occurring in patients with Alzheimer’s disease. By carefully examining the common genetic processes involved in these two diseases, these data may help unravel phenomena associated with the development of Alzheimer’s disease and neurodegeneration after cerebral ischemia and may lead future research on Alzheimer’s disease or cerebral ischemia in new directions.

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Upregulation of hemeoxygenase enzymes HO-1 and HO-2 following ischemia-reperfusion injury in connection with experimental cardiac arrest and cardiopulmonary resuscitation: Neuroprotective effects of methylene blue

Wiklund

Sharma

Patnaik

et al. 2021

Progress in Brain Research

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Motor Cortex and Hippocampus Display Decreased Heme Oxygenase Activity 2 Weeks After Ventricular Fibrillation Cardiac Arrest in Rats

Cited by 3 publications

References 75 publications

A resting-state functional magnetic resonance imaging study of altered functional brain activity in cardiac arrest survivors with good neurological outcome

A resting-state functional magnetic resonance imaging study of altered functional brain activity in cardiac arrest survivors with good neurological outcome

Ischemia-Reperfusion Programming of Alzheimer’s Disease-Related Genes—A New Perspective on Brain Neurodegeneration after Cardiac Arrest

Upregulation of hemeoxygenase enzymes HO-1 and HO-2 following ischemia-reperfusion injury in connection with experimental cardiac arrest and cardiopulmonary resuscitation: Neuroprotective effects of methylene blue

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