Cytidine 5′-diphosphocholine (CDP-choline) adversely effects on pilocarpine seizure-induced hippocampal neuronal death

Kim, Jin Hee; Lee, Jun Young; Choi, Bo Young; Sohn, Min; Lee, Song Hee; Choi, Hyeong‐Ah; Song, Heesang; Suh, Sang Won

doi:10.1016/j.brainres.2014.11.011

Cited by 13 publications

(13 citation statements)

References 50 publications

(50 reference statements)

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“…Larger molecular weight permeability markers include IRDye 800CW which can vary in size from 15 kDa and upwards, depending on conjugation [25]. Fluorescein isothiocyanate conjugated to dextran or albumin has been used, as well as probing for IgG penetration into the central nervous system after injury [26][27][28][29][30]. Two-photon microscopy with tetramethylrhodamine-dextran is less invasive, and has been used in rat and mouse models of stroke and neoplasia for in vivo cerebral blood flow and edema information [31].…”

Section: Preclinical Measurements Of Bbb Permeabilitymentioning

confidence: 99%

Assessing Blood Brain Barrier Permeability in Traumatic Brain Injury Research

et al. 2015

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The blood brain barrier plays an important role in traumatic brain injury, serving at the crossroads of secondary injury and potential therapies. In regards to trauma, this barrier contains an array of cellular and molecular components that protect the central nervous system from derangements in water homeostasis and inflammation. Preclinical and clinical assays have been developed to describe and quantify blood brain barrier permeability in relation to the integrity of these blood brain barrier components and the handling ofedema. This review will discuss both preclinical and clinical molecular and imaging techniques that are used to assess blood brain barrier function and recovery following traumatic brain injury.

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Section: Preclinical Measurements Of Bbb Permeabilitymentioning

confidence: 99%

Assessing Blood Brain Barrier Permeability in Traumatic Brain Injury Research

et al. 2015

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“…Severe and sustained seizures may lead to more serious events, such as hypoxia and excitotoxic neuronal damage when not treated properly. Furthermore, even timely intervention with anti-epileptic drugs has failed to prevent delayed neuronal death, which is correlated with cognitive decline [ 5 - 7 ]. For this reason, numerous in vivo studies have tested a multitude of neuroprotective agents for the prevention of progressive neuronal damage and subsequent cognitive impairment.…”

Section: Introductionmentioning

confidence: 99%

“…For this reason, numerous in vivo studies have tested a multitude of neuroprotective agents for the prevention of progressive neuronal damage and subsequent cognitive impairment. However, results have been inconsistent and difficult to interpret [ 5 , 7 - 10 ]. Therefore, continuous effort is needed to develop new, more effective treatment options.…”

Section: Introductionmentioning

confidence: 99%

Unexpected Effects of Acetylcholine Precursors on Pilocarpine Seizure- Induced Neuronal Death

Lee

Choi

Suh

2017

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Background:Choline alfoscerate (α-GPC) and Cytidine 5’-diphosphocholine (CDP-Choline) are both acetylcholine precursors and are considered to act as pro-cholinergic nootropic agents. Acetylcholine precursors have also recently found frequent use in the neurology clinic. Stroke and many types of dementia have been shown to respond favorably after treatment with these agents, not only in terms of cognitive dysfunction but also behavioral and psychological symptoms. The primary mechanisms of Acetylcholine precursors are the following: 1) Acetylcholine precursors themselves are used in the biosynthesis of acetylcholine and 2) byproducts like glycerophosphate have protective functions for neuronal phospholipids. However, whether acetylcholine precursors have a similar effect in treating cognitive impairment in patients with epilepsy remains controversial.Methods:Our previous studies investigating acetylcholine precursors in seizure-experienced animals have produced variable results that were dependent on the timing of administration.Results:Early administration of CDP-choline immediately after seizure increased neuronal death, blood-brain barrier (BBB) disruption and microglial activation in the hippocampus. However, administration of α-GPC starting 3 weeks after seizure (late administration) improved cognitive function through reduced neuronal death and BBB disruption, and increased neurogenesis in the hippocampus.Conclusion:These seemingly contradictory results may be attributed to both epileptogenic features and neuroprotective functions of several acetylcholine precursors.

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“…Our previous study showed that acetylcholine precursors such as citicoline and α–GPC demonstrated mixed effects on seizure behavior and seizure-induced neuronal death [ 20 , 21 , 22 ]. Citicoline and α–GPC both increased seizure-induced neuronal death if injected immediately after the seizure.…”

Section: Introductionmentioning

confidence: 99%

Diverse Effects of an Acetylcholinesterase Inhibitor, Donepezil, on Hippocampal Neuronal Death after Pilocarpine-Induced Seizure

Jeong

Choi

Kho

et al. 2017

IJMS

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Epileptic seizures are short episodes of abnormal brain electrical activity. Many survivors of severe epilepsy display delayed neuronal death and permanent cognitive impairment. Donepezil is an acetylcholinesterase inhibitor and is an effective treatment agent for Alzheimer’s disease. However, the role of donepezil in seizure-induced hippocampal injury remains untested. Temporal lobe epilepsy (TLE) was induced by intraperitoneal injection of pilocarpine (25 mg/kg). Donepezil (2.5 mg/kg/day) was administered by gavage in three different settings: (1) pretreatment for three days before the seizure; (2) for one week immediately after the seizure; and (3) for three weeks from three weeks after the seizure. We found that donepezil showed mixed effects on seizure-induced brain injury, which were dependent on the treatment schedule. Pretreatment with donepezil aggravated neuronal death, oxidative injury, and microglia activation. Early treatment with donepezil for one week showed neither adverse nor beneficial effects; however, a treatment duration of three weeks starting three weeks after the seizure showed a significant reduction in neuronal death, oxidative injury, and microglia activation. In conclusion, donepezil has therapeutic effects when injected for three weeks after seizure activity subsides. Therefore, the present study suggests that the therapeutic use of donepezil for epilepsy patients requires a well-conceived strategy for administration.

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Cytidine 5′-diphosphocholine (CDP-choline) adversely effects on pilocarpine seizure-induced hippocampal neuronal death

Cited by 13 publications

References 50 publications

Assessing Blood Brain Barrier Permeability in Traumatic Brain Injury Research

Assessing Blood Brain Barrier Permeability in Traumatic Brain Injury Research

Unexpected Effects of Acetylcholine Precursors on Pilocarpine Seizure- Induced Neuronal Death

Diverse Effects of an Acetylcholinesterase Inhibitor, Donepezil, on Hippocampal Neuronal Death after Pilocarpine-Induced Seizure

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