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9 Choline
Pages 115-129

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From page 115...
... . Although there are no human studies examining the effect of supplementation during pregnancy on enhanced memory of the newborn, there are animal studies showing that choline supplementation provided during hippocampal development has an effect on maintaining memory in older age.
From page 116...
... Inhibiting caspase activity may decrease apoptotic activity and calcium-mediated cell death. Supporting these ideas, in vitro studies have also revealed that choline deficiency induces apoptosis in the liver by mechanisms independent of protein 53, which likely involve abnormal mitochondrial membrane phosphatidylcholine, leakage of oxygen radicals, and activation of caspases (Albright and Zeisel, 1997; Albright et al., 1996, 1998, 1999a, 199b, 2003; Chen et al., 2010)
From page 117...
... evaluating the effectiveness of CDP-choline in providing resilience or treating TBI or related diseases or conditions (i.e., subarachnoid hemorrhage, intracranial aneurysm, stroke, anoxic or hypoxic ischemia, epilepsy) in the acute phase in humans is presented in Table 9-1; this also includes supporting evidence from animal models of TBI.
From page 118...
... . In patients with NIHSS (National Institutes of Health Stroke Scale)
From page 119...
... ; 6-week treatment (52%) groups showed a 7-point NIHSS ≥ 8 efficacy trial treatment, 6-week improvement on their NIHSS scores.
From page 120...
... . Clark et al., Acute Randomized, Postinjury, Post hoc analyses found that among patients with baseline NIHSS ≥ 8, CDP1999 ischemic double-blind, oral CDP-choline stroke, efficacy trial at (500 mg/day)
From page 121...
... improved on Rankin Scale score. Treatment effect on cognitive function (MMSE ≥ 25)
From page 122...
... . postinjury and 6 hours postinjury Treatment with 200 mg/kg and 400 mg/kg of CDP-choline also reduced the volume of cortical contusion by 21 mm3 (p < 0.05)
From page 123...
... for two groups in both tasks was minimized 18 days, beginning by day 4. 1 day postinjury CDP-choline treated rats also had shorter latency in completing the Morris water maze than saline-treated rats (p < 0.005)
From page 124...
... A major mechanism of secondary injury in TBI is the formation of reactive oxygen species and lipid peroxidases, which cause significant tissue damage. Animal models of TBI support a key role for oxidative stress (Ikeda and Long, 1990; Kontos et al., 1992)
From page 125...
... , suggesting that CDP-choline enhances cholinergic transmission and may ameliorate chronic functional deficits. A second mechanism that may explain why CDP-choline improves function in chronically injured animals focuses on observed decreases in dopamine following injury (Yan et al., 2001)
From page 126...
... If ongoing trials with CDP-choline and TBI patients show positive results, further studies are warranted to confirm the optimal duration of treatment and clinical dose of choline for injured patients. Likewise, if those studies reveal that choline is a promising intervention, the effect of choline supplementation prior to injury to improve resilience could be explored by conducting animal studies.
From page 127...
... 2003. Cytidinediphosphocholine treatment to decrease traumatic brain injury-induced hippocampal neuronal death, cortical contusion volume, and neurological dysfunction in rats.
From page 128...
... 2002. CDP-choline reduces pro caspase and cleaved caspase-3 expression, nuclear DNA fragmentation, and specific PARP-cleaved products of caspase activation following middle cerebral artery occlusion in the rat.
From page 129...
... 2010. Water maze experience and prenatal choline supplementation differentially promote long-term hippocampal recovery from seizures in adulthood.


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