Effects of CDP-choline on the recovery of patients with head injury

Maldonado, V. Calatayud; Pérez, Juan Bosco Calatayud; Escario, J. Aso

doi:10.1016/0022-510x(91)90003-p

Cited by 54 publications

(17 citation statements)

References 2 publications

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“…Apart from inhibition of PLA2 activity, CDP-choline also stimulates synthesis of phosphatidylcholine (Grieb, 2014). Despite promising results in TBI and stroke models and in small clinical studies (Calatayud Maldonado et al, 1991; Clark et al, 1997; Clark et al, 1999; Clark et al, 2001; Davalos et al, 2002; Tazaki et al, 1988) two recent large clinical trials showed no benefit in TBI and ischemic stroke (Zafonte et al, 2012; Davalos et al, 2012). It is worth mentioning that glycosphingolipids, primarily gangliosides, strongly inhibit PLA2 activity ex vivo (Bianco et al, 1989), thus they have been tested for their neuroprotective potential in a number of CNS injury models (Sabel et al, 1984) (Toffano et al, 1984) as well as in patients with spinal cord injury.…”

Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

Therapies targeting lipid peroxidation in traumatic brain injury

2016

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Lipid peroxidation can be broadly defined as the process of inserting a hydroperoxy group into a lipid. Polyunsaturated fatty acids present in the phospholipids are often the targets for peroxidation. Phospholipids are indispensable for normal structure of membranes. The other important function of phospholipids stems from their role as a source of lipid mediators – oxygenated free fatty acids that are derived from lipid peroxidation. In the CNS, excessive accumulation of either oxidized phospholipids or oxygenated free fatty acids may be associated with damage occurring during acute brain injury and subsequent inflammatory responses. There is a growing body of evidence that lipid peroxidation occurs after severe traumatic brain injury in humans and correlates with the injury severity and mortality. Identification of the products and sources of lipid peroxidation and its enzymatic or non-enzymatic nature is essential for the design of mechanism-based therapies. Recent progress in mass spectrometry-based lipidomics/oxidative lipidomics offers remarkable opportunities for quantitative characterization of lipid peroxidation products, providing guidance for targeted development of specific therapeutic modalities. In this review, we critically evaluate previous attempts to use non-specific antioxidants as neuroprotectors and emphasize new approaches based on recent breakthroughs in understanding of enzymatic mechanisms of lipid peroxidation associated with specific death pathways, particularly apoptosis. We also emphasize the role of different phospholipases (calcium-dependent and -independent) in hydrolysis of peroxidized phospholipids and generation of pro- and anti-inflammatory lipid mediators.

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Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

Therapies targeting lipid peroxidation in traumatic brain injury

2016

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“…Six of eight trials using physical rehabilitation also showed positive treatment effects, and nutrition and acupuncture were found to be beneficial in the single trials conducted thus far. Potential TBI pharmacotherapies were tested in 11 post-acute RCTs, with positive treatment effects reported in six studies, including for methylphenidate (Whyte et al, 2004; Willmott and Ponsford, 2009), CDP-choline (Calatayud Maldonado et al, 1991) and pyritinol (Kitamura, 1981). A trial of phenytoin and carbamazepine was negative (Smith et al, 1994), and sertraline, carbamazepine, rivsatigmine and modafinil were found to have no significant treatment effects (Banos et al, 2010; Jha et al, 2008; Novack et al, 2009; Tenovuo et al, 2009).…”

Section: Pathophysiology Classification and Clinical Management Of Tbimentioning

confidence: 99%

Towards clinical management of traumatic brain injury: a review of models and mechanisms from a biomechanical perspective

Namjoshi

Good²,

Cheng

et al. 2013

Disease Models &Amp; Mechanisms

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Traumatic brain injury (TBI) is a major worldwide healthcare problem. Despite promising outcomes from many preclinical studies, the failure of several clinical studies to identify effective therapeutic and pharmacological approaches for TBI suggests that methods to improve the translational potential of preclinical studies are highly desirable. Rodent models of TBI are increasingly in demand for preclinical research, particularly for closed head injury (CHI), which mimics the most common type of TBI observed clinically. Although seemingly simple to establish, CHI models are particularly prone to experimental variability. Promisingly, bioengineering-oriented research has advanced our understanding of the nature of the mechanical forces and resulting head and brain motion during TBI. However, many neuroscience-oriented laboratories lack guidance with respect to fundamental biomechanical principles of TBI. Here, we review key historical and current literature that is relevant to the investigation of TBI from clinical, physiological and biomechanical perspectives, and comment on how the current challenges associated with rodent TBI models, particularly those involving CHI, could be improved.

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“…In Europe, Asia, and more recently in the United States, citicoline has been used to treat human patients for ischemia as a result of traumatic brain injury (Spiers and Hochanadel, 1999; Baskaya et al, 2000) or stroke (Cho and Kim, 2009). After citicoline treatment, the volume of ischemic lesions are reduced, and structural integrity of the brain, levels of consciousness, neurological symptoms, motor deficits, hypertonia, psychomotor function, EEG activity, and general quality of life are all improved over placebo treatment (Calatayud Maldonado et al, 1991; Levin, 1991; Warach et al, 2000; Clark et al, 2001; Davalos et al, 2002). If citicoline treatment in cocaine dependent individuals is as effective at normalizing neuronal membrane phospholipids as it is in brain injury patients, citicoline may augment the ability of the brain to repair itself in these individuals during sustained cocaine abstinence.…”

Section: Introductionmentioning

confidence: 99%

Eight weeks of citicoline treatment does not perturb sleep/wake cycles in cocaine-dependent adults

Bracken¹,

Penetar²,

Rodolico³

et al. 2011

Pharmacology Biochemistry and Behavior

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Background Citicoline (cytidine-5’-diphosphate) is a mononucleotide composed of ribose, cytosine, pyrophosphate, and choline, and is involved in the biosynthesis of the structural phosopholipids of cell membranes. Treatment with citicoline, improves memory in patients with dementia, and reduces damage to the brain after traumatic brain injury or stroke. Recent research has been conducted to assess whether citicoline is an effective treatment for cocaine dependence. In cocaine-dependent individuals, withdrawal from cocaine is associated with disturbed sleep, which may contribute to the high rate of relapse to cocaine use. Therefore, it is important to know the impact of citicoline on the sleep/wake cycle in these individuals in order to rate its overall efficacy. Method In this double-blind, placebo-controlled trial, the effects of citicoline treatment on the sleep/wake cycles of cocaine dependent participants were assessed. The results of the current study are reported as part of a larger study, consisting of an eight-week treatment period to assess the efficacy of longer-term treatment with citicoline at decreasing cocaine consumption in cocaine-dependent polydrug using participants. Results In this non-abstinent, cocaine-dependent population, citicoline had no effect on any of the sleep parameters measured including sleep efficiency, sleep latency, total sleep time, number of waking episodes, time awake per episode, amount of time in bed spent moving, number of sleep episodes, time asleep per episode, and amount of time in bed spent immobile. Conclusions These data suggest that eight weeks of citicoline administration does not disturb sleep/wake cycles of cocaine-dependent individuals.

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Effects of CDP-choline on the recovery of patients with head injury

Cited by 54 publications

References 2 publications

Therapies targeting lipid peroxidation in traumatic brain injury

Therapies targeting lipid peroxidation in traumatic brain injury

Towards clinical management of traumatic brain injury: a review of models and mechanisms from a biomechanical perspective

Eight weeks of citicoline treatment does not perturb sleep/wake cycles in cocaine-dependent adults

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