An overview of evidence for a causal relationship between dietary availability of choline during development and cognitive function in offspring

McCann, Joyce C.; Hudes, Mark; Ames, Bruce N.

doi:10.1016/j.neubiorev.2005.12.003

Cited by 133 publications

(113 citation statements)

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“…Enhanced hippocampal plasticity likely plays a significant role in both the memory-enhancing effects of prenatal choline supplementation (Meck & Williams, 2003;McCann et al, 2006) and its neuroprotective actions. Much like our prenatal choline supplemented adult rats, juvenile rats that experience SE also show resistance to seizure-induced hippocampal cell loss, disinhibition, and mossy fiber sprouting (Sperber et al, 1991;Haas et al, 2001), and exhibit savings in spatial learning and memory (Stafstrom et al, 1993;Sarkisian et al, 1997) when compared to adult rats that experience SE.…”

Section: Discussionmentioning

confidence: 99%

“…Prenatal and early postnatal choline supplementation has also been shown to protect against impairments in performance on hippocampal-dependent tasks caused by aging (Meck et al, 1988(Meck et al, , 1989Meck & Williams, 2003;McCann et al, 2006) or neonatal alcohol exposure (Thomas et al, 2004(Thomas et al, , 2007Wagner & Hunt, 2006). While the mechanism by which prenatal choline supplementation confers neuroprotection is not fully understood, choline is a vital nutrient important for several biological functions: acetylcholine synthesis, building biological membranes, cell signaling, and methyl donation (Blusztajn, 1998;Zeisel, 2004Zeisel, , 2006.…”

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confidence: 99%

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Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

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Prenatal choline supplementation (SUP) protects adult rats against spatial memory deficits observed after excitotoxin-induced status epilepticus (SE). To examine the mechanism underlying this neuroprotection, we determined the effects of SUP on a variety of hippocampal markers known to change in response to SE and thought to underlie ensuing cognitive deficits. Adult offspring from rat dams that received either a Control or SUP diet on embryonic days 12-17 were administered saline or kainic acid (i.p.) to induce SE and were euthanized 16 days later. SUP markedly attenuated seizure-induced hippocampal neurodegeneration, dentate cell proliferation, hippocampal GFAP mRNA expression levels, prevented the loss of hippocampal GAD65 protein and mRNA expression, and altered growth factor expression patterns. SUP also enhanced pre-seizure hippocampal levels of BDNF, NGF, and IGF-1, which may confer a neuroprotective hippocampal microenvironment that dampens the neuropathological response to and/or helps facilitate recovery from SE to protect cognitive function. Keywords choline; kainic acid; hippocampus; seizures; bromodeoxyuridine; growth factor; glutamic acid decarboxylase; glial fibrillary acidic protein; neuroprotection Status epilepticus (SE), a period of prolonged seizures, produces a host of plastic changes in the hippocampus that are thought to contribute to the development of temporal lobe epilepsy. SE results in substantial neuronal loss (Cavazos et al., 1994;Haas et al., 2001;Gorter et al., 2003), γ-aminobutyric acid (GABA) system alterations (e.g., Houser & Esclapez, 1996), reactive gliosis (Jorgensen et al. 1993; Niquet et al., 1994a;Kang et al., 2006), mossy fiber innervation of the dentate gyrus (Sutula et al., 1988;Ben-Ari & Represa, 1990), changes in levels of growth factors (Khrestchatisky et al., 1995;Mudo et al., 1996;Schmidt-Kastner et al., 1996;Shetty et al., 2004), and a transient increase in cell proliferation and neurogenesis (Bengzon et al., 1997;Parent et al., 1997;Scharfman et al., 2000;Hattiangady et al., 2004). These SE-induced degenerative and regenerative changes in the hippocampus are also Corresponding author: Dr. Christina L. Williams, Department of Psychology and Neuroscience, 572 Research Drive, Box 91050, GSRB-II, Room 3022, Duke University, Durham, NC 27708, USA, Phone: 919-660-5638, Fax: 919-660-5798, Email: williams@psych.duke.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. accompanied by deficits in hippocampal-dependent learning and memory (Stafstrom et al., 1993;Liu et al., 1994;Sarkisian et al., 1997;Hort et al., 1999;Mik...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

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“…Studies in animal models (2)(3)(4)(5) as well as recent epidemiological investigations in humans (6) indicate that choline intake during gestation is particularly important for the normal development and function of the central nervous system. In a frequently used experimental model that employs offspring of pregnant rats or mice consuming diets of varying choline content during the 7-day period of the second half of gestation (embryonic days E11-17), prenatal choline deficiency causes deficits in certain memory tasks (7), whereas prenatal choline supplementation leads to enhanced memory and attention and prevents agerelated memory decline (7)(8)(9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

“…In a frequently used experimental model that employs offspring of pregnant rats or mice consuming diets of varying choline content during the 7-day period of the second half of gestation (embryonic days E11-17), prenatal choline deficiency causes deficits in certain memory tasks (7), whereas prenatal choline supplementation leads to enhanced memory and attention and prevents agerelated memory decline (7)(8)(9)(10)(11)(12)(13). These behavioral changes are accompanied by electrophysiological, neuroanatomical, and neurochemical alterations that persist in the adulthood and old age (2)(3)(4)(5) and, remarkably, by altered patterns of brain gene expression postnatally (14). Although the molecular mechanisms for these long-term effects of prenatal choline intake are not known, it is possible that they are related to the function of choline as a methyl group donor in one of the two alternative pathways that produce methionine by scavenging homocysteine.…”

mentioning

confidence: 99%

Gestational Choline Deficiency Causes Global and Igf2 Gene DNA Hypermethylation by Up-regulation of Dnmt1 Expression

Kovacheva

Mellott

Davison

et al. 2007

Journal of Biological Chemistry

212

191

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During gestation there is a high demand for the essential nutrient choline. Adult rats supplemented with choline during embryonic days (E) 11-17 have improved memory performance and do not exhibit age-related memory decline, whereas prenatally choline-deficient animals have memory deficits. Choline, via betaine, provides methyl groups for the production of S-adenosylmethionine, a substrate of DNA methyltransferases (DNMTs). We describe an apparently adaptive epigenomic response to varied gestational choline supply in rat fetal liver and brain. S-Adenosylmethionine levels increased in both organs of E17 fetuses whose mothers consumed a choline-supplemented diet. Surprisingly, global DNA methylation increased in choline-deficient animals, and this was accompanied by overexpression of Dnmt1 mRNA. Previous studies showed that the prenatal choline supply affects the expression of multiple genes, including insulin-like growth factor 2 (Igf2), whose expression is regulated in a DNA methylation-dependent manner. The differentially methylated region 2 of Igf2 was hypermethylated in the liver of E17 choline-deficient fetuses, and this as well as Igf2 mRNA levels correlated with the expression of Dnmt1 and with hypomethylation of a regulatory CpG within the Dnmt1 locus. Moreover, mRNA expression of brain and liver Dnmt3a and methyl CpG-binding domain 2 (Mbd2) protein as well as cerebral Dnmt3l was inversely correlated to the intake of choline. Thus, choline deficiency modulates fetal DNA methylation machinery in a complex fashion that includes hypomethylation of the regulatory CpGs within the Dnmt1 gene, leading to its overexpression and the resultant increased global and gene-specific (e.g. Igf2) DNA methylation. These epigenomic responses to gestational choline supply may initiate the long term developmental changes observed in rats exposed to varied choline intake in utero.An adequate supply of essential nutrients involved in the metabolism of methyl groups, including folic acid, vitamin B 12 , and choline, is central for normal development of the fetus. This is perhaps best exemplified by the discovery that the dietary supply of folic acid, a vitamin that acts as a coenzyme in one-carbon transfer pathways, during the periconceptual period is critical in prevention of neural tube defects (1). Studies in animal models (2-5) as well as recent epidemiological investigations in humans (6) indicate that choline intake during gestation is particularly important for the normal development and function of the central nervous system. In a frequently used experimental model that employs offspring of pregnant rats or mice consuming diets of varying choline content during the 7-day period of the second half of gestation (embryonic days E11-17), prenatal choline deficiency causes deficits in certain memory tasks (7), whereas prenatal choline supplementation leads to enhanced memory and attention and prevents agerelated memory decline (7-13). These behavioral changes are accompanied by electrophysiological, neuroanatomical, and neuro...

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“…Some other experiments also conducted in children, showed improvement of motor and neuropsychological outcomes after iron supplementation, while others have found no effects; even though, these results are inconsistent, the favorable benefits acquired from preventing deficits are prevalent. Thus, the importance of protecting the developing brain from early iron deprivation is highly emphasized (122,123).…”

Section: Mineralsmentioning

confidence: 99%

Nutritional strategies in the management of Alzheimer\'s disease: systematic review and meta-analysis

Fernández¹,

Steffany²

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An overview of evidence for a causal relationship between dietary availability of choline during development and cognitive function in offspring

Cited by 133 publications

References 117 publications

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Gestational Choline Deficiency Causes Global and Igf2 Gene DNA Hypermethylation by Up-regulation of Dnmt1 Expression

Nutritional strategies in the management of Alzheimer\'s disease: systematic review and meta-analysis

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