Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [<sup>18</sup>F] VAT positron emission tomography brain imaging study

Wu, Xuqing; Ding, Jing; Si, Zhan; Cheng, Dengfeng; Shi, Hongcheng; Wang, Xin

doi:10.1111/epi.14533

Cited by 8 publications

(4 citation statements)

References 38 publications

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“…Disruption of this activity through pathological processes (e.g., the generation of epileptic spikes) may be a significant mechanism underlying the pathogenesis and cognitive deficits in epilepsy. Centres in China have engaged in research in this field and some pioneering findings have been reported [82][83][84][85][86][87][88][89][90] . Temporal lobe epilepsy (TLE) with hippocampal sclerosis is the most common type of drug-resistant epilepsy.…”

Section: Epilepsy Researchmentioning

confidence: 99%

Epilepsy in China: major progress in the past two decades

Ding

Zhou

Sander

et al. 2021

The Lancet Neurology

103

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China has about 10 million people with epilepsy. A vast 'epilepsy treatment gap' in China mainly driven by deficiencies in healthcare delivery and social discrimination resulting from cultural beliefs about epilepsy. The WHO's Global Campaign against Epilepsy Demonstration Project in China, which showed that it was possible to treat epilepsy in primary care, was a significant milestone. The China Association against Epilepsy has been a vital force to stimulate epilepsy interest. Nearly 20 anti-seizure medications are available in China. Non-pharmacological options are available, but they are still unmet needs for epilepsy management. The Chinese epilepsy research portfolio is varied, but areas of concentration and thus, expertise are particularly in epidemiology and clinical research. The challenges remaining for further improvement for delivering care for people with epilepsy in China are primarily related to public health and to reducing inequalities within this vast country.

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Section: Epilepsy Researchmentioning

confidence: 99%

Epilepsy in China: major progress in the past two decades

Ding

Zhou

Sander

et al. 2021

The Lancet Neurology

103

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“…Schildt et al suggested that the discrepancy between raclopride and haloperidol pre-treatment effects was due to haloperidol blockade of off-target [ 18 F]FEOBV binding to σ receptors. This seems unlikely as brain [ 18 F]FEOBV uptake is not affected by pre-treatment with the σ antagonist (+)-3-PPP, the strong concordance between regional distribution of [ 18 F]FEOBV binding revealed in human PET studies and prior post-mortem based characterizations of the organization of human brain cholinergic systems, and results of rodent lesion experiments correlating ex vivo measurements of cholinergic systems integrity with in vivo [ 18 F]FEOBV and [ 18 F]VAT PET measurements. − In addition, FEOBV has a low affinity for the human σ 1 receptor…”

Section: Discussionmentioning

confidence: 99%

No Dopamine Agonist Modulation of Brain [¹⁸F]FEOBV Binding in Parkinson’s Disease

et al. 2022

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The [ 18 F]fluoroethoxybenzovesamicol ([ 18 F]-FEOBV) positron emission tomography (PET) ligand targets the vesicular acetylcholine transporter. Recent [ 18 F]FEOBV PET rodent studies suggest that regional brain [ 18 F]FEOBV binding may be modulated by dopamine D2-like receptor agents. We examined associations of regional brain [ 18 F]FEOBV PET binding in Parkinson's disease (PD) subjects without versus with dopamine D2-like receptor agonist drug treatment. PD subjects (n = 108; 84 males, 24 females; mean age 68.0 ± 7.6 [SD] years), mean disease duration of 6.0 ± 4.0 years, and mean Movement Disorder Societyrevised Unified PD Rating Scale III 35.5 ± 14.2 completed [ 18 F]FEOBV brain PET imaging. Thirty-eight subjects were taking dopamine D2-like agonists. Vesicular monoamine transporter type 2 [ 11 C]dihydrotetrabenazine (DTBZ) PET was available in a subset of 54 patients. Subjects on dopamine D2-like agonists were younger, had a longer duration of disease, and were taking a higher levodopa equivalent dose (LED) compared to subjects not taking dopamine agonists. A group comparison between subjects with versus without dopamine D2-like agonist use did not yield significant differences in cortical, striatal, thalamic, or cerebellar gray matter [ 18 F]FEOBV binding. Confounder analysis using age, duration of disease, LED, and striatal [ 11 C]DTBZ binding also failed to show significant regional [ 18 F]FEOBV binding differences between these two groups. Chronic D2-like dopamine agonist use in PD subjects is not associated with significant alterations of regional brain [ 18 F]FEOBV binding.

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“…Alteration of VAChT expression has consequences on the concentration of acetylcholine loaded in the secretory vehicle, thus indirectly maintaining the neurotransmitter release. Dysregulation of VAChT has been reported in several diseases like AD, Epilepsy, and Sepsis (117)(118)(119). VAChT knockdown (VAChT-KD) mice, upon LPS challenge, show increased susceptibility to inflammation and greater mortality.…”

Section: Rivastigminementioning

confidence: 99%

Cholinergic System and Its Therapeutic Importance in Inflammation and Autoimmunity

Halder

Lal

2021

Front. Immunol.

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Neurological and immunological signals constitute an extensive regulatory network in our body that maintains physiology and homeostasis. The cholinergic system plays a significant role in neuroimmune communication, transmitting information regarding the peripheral immune status to the central nervous system (CNS) and vice versa. The cholinergic system includes the neurotransmitter\ molecule, acetylcholine (ACh), cholinergic receptors (AChRs), choline acetyltransferase (ChAT) enzyme, and acetylcholinesterase (AChE) enzyme. These molecules are involved in regulating immune response and playing a crucial role in maintaining homeostasis. Most innate and adaptive immune cells respond to neuronal inputs by releasing or expressing these molecules on their surfaces. Dysregulation of this neuroimmune communication may lead to several inflammatory and autoimmune diseases. Several agonists, antagonists, and inhibitors have been developed to target the cholinergic system to control inflammation in different tissues. This review discusses how various molecules of the neuronal and non-neuronal cholinergic system (NNCS) interact with the immune cells. What are the agonists and antagonists that alter the cholinergic system, and how are these molecules modulate inflammation and immunity. Understanding the various functions of pharmacological molecules could help in designing better strategies to control inflammation and autoimmunity.

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Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [¹⁸F] VAT positron emission tomography brain imaging study

Abstract: [ F] VAT PET is a promising method to test the level of VAChT as a valuable biomarker for memory deficits in pilocarpine-induced chronic epileptic rats.

Cited by 8 publications

References 38 publications

Epilepsy in China: major progress in the past two decades

Epilepsy in China: major progress in the past two decades

No Dopamine Agonist Modulation of Brain [¹⁸F]FEOBV Binding in Parkinson’s Disease

Cholinergic System and Its Therapeutic Importance in Inflammation and Autoimmunity

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Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [18F] VAT positron emission tomography brain imaging study

Abstract: [ F] VAT PET is a promising method to test the level of VAChT as a valuable biomarker for memory deficits in pilocarpine-induced chronic epileptic rats.

Cited by 8 publications

References 38 publications

Epilepsy in China: major progress in the past two decades

Epilepsy in China: major progress in the past two decades

No Dopamine Agonist Modulation of Brain [18F]FEOBV Binding in Parkinson’s Disease

Cholinergic System and Its Therapeutic Importance in Inflammation and Autoimmunity

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Product

Resources

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Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [¹⁸F] VAT positron emission tomography brain imaging study

No Dopamine Agonist Modulation of Brain [¹⁸F]FEOBV Binding in Parkinson’s Disease