Record 1 from database: MEDLINE
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- Title
- Brain choline has a typical precursor profile.
- Author
- Löffelholz K
- Address
- Department of Pharmacology, University of Mainz,
Germany.
- Source
- J Physiol Paris, 1998 Jun, 92:3-4, 235-9
- Abstract
- Choline is product and precursor to both acetylcholine
and membrane phospholipids, and, in the brain, is
ultimately provided by the circulation. The brain is
protected from excess choline and choline deprivation by
a refined system of homeostatic mechanisms that maintain
a level of extracellular choline that, for its role as
precursor, meets saturation criteria under normal
conditions. The kinetic and activity profiles of choline
are typical for a biosynthetic precursor.
- Language of Publication
- English
- Unique Identifier
- 99006244
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- MeSH Heading (Major)
- Acetylcholine|*BI; Brain|*ME; Choline|*ME;
Phospholipids|*BI
- MeSH Heading
- Animal; Homeostasis; Human; Kinetics; Support,
Non-U.S. Gov't; Synapses|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0928-4257
- Country of Publication
- FRANCE
Record 2 from database: MEDLINE
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- Title
- Dietary Reference Intakes: the new basis for
recommendations for calcium and related nutrients, B
vitamins, and choline.
- Author
- Yates AA; Schlicker SA; Suitor CW
- Address
- Food and Nutrition Board, Institute of Medicine,
National Academy of Sciences, Washington, DC 20418, USA.
- Source
- J Am Diet Assoc, 1998 Jun, 98:6, 699-706
- Abstract
- Dietary Reference Intakes (DRIs) represent the new
approach adopted by the Food and Nutrition Board to
providing quantitative estimates of nutrient intakes for
use in a variety of settings, replacing and expanding on
the past 50 years of periodic updates and revisions of
the Recommended Dietary Allowances (RDAs). The DRI
activity is a comprehensive effort undertaken to include
current concepts about the role of nutrients and food
components in long-term health, going beyond deficiency
diseases. The DRIs consist of 4 reference intakes: the
RDA, which is to be used as a goal for the individual;
the Tolerable Upper Intake Level (UL), which is given to
assist in advising individuals what levels of intake may
result in adverse effects if habitually exceeded; the
Estimated Average Requirement (EAR), the intake level at
which the data indicate that the needs for 50% of those
consuming it will not be met; and the Adequate Intake
(AI), a level judged by the experts developing the
reference intakes to meet the needs of all individuals
in a group, but which is based on much less data and
substantially more judgment than that used in
establishing an EAR and subsequently the RDA. When an
RDA cannot be set, an AI is given. Both are to be used
as goals for an individual. Two reports have been issued
providing DRIs for nutrients and food components
reviewed to date: these include calcium and its related
nutrients: phosphorus, magnesium, vitamin D, and
fluoride; and most recently, folate, the B vitamins, and
choline. The approaches used to determine the DRIs, the
reference values themselves, and the plans for future
nutrients and food components are discussed.
- Language of Publication
- English
- Unique Identifier
- 98291100
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- MeSH Heading (Major)
- Guidelines|*; National Academy of Sciences (U.S.)|*;
Nutrition Policy|*
- MeSH Heading
- Calcium, Dietary|AD; Choline|AD; Human; Reference
Values; Support, Non-U.S. Gov't; Support, U.S. Gov't,
Non-P.H.S.; Support, U.S. Gov't, P.H.S.; United States;
Vitamin B Complex|AD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-8223
- Country of Publication
- UNITED STATES
Record 3 from database: MEDLINE
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- Title
- Choline: essential for brain development and function.
- Author
- Zeisel SH
- Address
- Department of Nutrition, School of Public Health and
School of Medicine, University of North Carolina, Chapel
Hill, USA.
- Source
- Adv Pediatr, 1997, 44:, 263-95
- Abstract
- Pregnancy and lactation are periods when maternal
reserves of choline are depleted. At the same time, the
availability of choline for normal development of brain
is critical. Variations in choline intake by mothers
influence memory performance in their offspring. The
mechanisms for this potent effect of choline are not yet
elucidated but may involve changes in acetylcholine
synthesis, transmembrane signal transduction, or
regulation of apoptosis. These observations are
important for the obstetrician and pediatrician as they
consider the ideal dietary intake for mothers and their
children.
- Language of Publication
- English
- Unique Identifier
- 97410924
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- MeSH Heading (Major)
- Brain|EM/*GD; Choline|*PH; Choline Deficiency|*PP;
Pregnancy Complications|*PP
- MeSH Heading
- Acetylcholine|ME; Animal; Apoptosis|PH; Female; Human;
Infant, Newborn; Lactation|ME; Pregnancy; Rats; Signal
Transduction|PH; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0065-3101
- Country of Publication
- UNITED STATES
Record 4 from database: MEDLINE
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- Title
- Essential nature of choline with implications for
total parenteral nutrition.
- Author
- Shronts EP
- Address
- Department of Surgery, University of Minnesota,
Minneapolis 55455, USA.
- Source
- J Am Diet Assoc, 1997 Jun, 97:6, 639-46, 649; quiz
647-8
- Abstract
- Choline is known to be important in many metabolic
pathways; at this time, however, it is not considered an
essential nutrient for human beings. Current evidence
strongly suggests that choline is "conditionally
essential," particularly for patients receiving
total parenteral nutrition (TPN). Studies in patients
receiving long-term TPN have shown that low levels of
plasma choline are common and can be associated with
hepatic steatosis. Treatment of these patients with oral
administration of choline improved plasma levels and
decreased hepatic fat content; however, oral choline
supplements are associated with poor compliance. More
recently, investigators have evaluated intravenous
administration of choline as a treatment for TPN-associated
hepatic steatosis in patients with documented subnormal
plasma free-choline levels. Initial results indicate
that intravenous administration of choline may be an
effective treatment for TPN-associated hepatic
dysfunction.
- Language of Publication
- English
- Unique Identifier
- 97326505
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- MeSH Heading (Major)
- Choline|AD/*ME/TU; Fatty Liver|BL/DT/*ET; Parenteral
Nutrition, Total|*AE
- MeSH Heading
- Administration, Oral; Clinical Trials; Dietetics|ED;
Dose-Response Relationship, Drug; Human; Injections,
Intravenous; Lipids|AN; Liver|CH/ME/PP; Questionnaires;
Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-8223
- Country of Publication
- UNITED STATES
Record 5 from database: MEDLINE
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- Title
- Antioxidants, carnitine, and choline as putative
ergogenic aids.
- Author
- Kanter MM; Williams MH
- Address
- Gatorade Sports Science Institute, Barrington, IL
60010, USA.
- Source
- Int J Sport Nutr, 1995 Jun, 5 Suppl:, S120-31
- Abstract
- Three nutritional products that have very different
mechanisms of action are antioxidant vitamins,
carnitine, and choline. Antioxidant vitamins do not
appear to have a direct effect on physical performance
in well-fed people but have been touted for their
ability to detoxify potentially damaging free radicals
produced during exercise. Carnitine purportedly enhances
lipid oxidation, increases VO2max, and decreases plasma
lactate accumulation during exercise. However, studies
of carnitine do not generally support its use for
ergogenic purposes. Choline supplements have been
advocated as a means of preventing the decline in
acetylcholine production purported to occur during
exercise; this decline may reduce the transmission of
contraction-generating impulses across the skeletal
muscle, an effect that could impair one's ability to
perform muscular work. However, there are no definitive
studies in humans that justify choline supplementation.
Much of the scientific data regarding the aforementioned
nutrients are equivocal and contradictory. Their
potential efficacy for improving physical performance
remains largely theoretical.
- Language of Publication
- English
- Unique Identifier
- 96018082
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- MeSH Heading (Major)
- Antioxidants|AD/*PD; Carnitine|AD/*PD; Choline|AD/*PD;
Exertion|*DE/PH
- MeSH Heading
- Acetylcholine|ME; Food, Fortified; Human; Muscle,
Skeletal|PH; Oxygen Consumption|PH
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1050-1606
- Country of Publication
- UNITED STATES
Record 6 from database: MEDLINE
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- Title
- High affinity choline transporter status in
Alzheimer's disease tissue from rapid autopsy.
- Author
- Bissette G; Seidler FJ; Nemeroff CB; Slotkin TA
- Address
- Department of Psychiatry, Duke University Medical
Center, Durham, North Carolina 27710, USA.
- Source
- Ann N Y Acad Sci, 1996 Jan, 777:, 197-204
- Abstract
- The degeneration of nucleus basalis cholinergic
neurons in Alzheimers disease (AD) has led to therapies
that attempt to increase the synaptic availability of
acetylcholine in the remaining cholinergic nerve
terminals and to thereby reverse or slow the progressive
dementia accompanying the disease process. The
inadequacy of current choline-replacement therapies
suggests that utilization of choline may be disordered
and the rate-limiting step in acetylcholine synthesis,
the high affinity choline transporter, may be involved.
An adequate test of this hypothesis requires the use of
fresh, unfrozen tissue, as the transporter activity
declines rapidly after death. Using tissue acquired
within two hours of death, the activity of the high
affinity choline transporter was shown to be increased
in cortical brain regions from AD patients compared to
non-AD controls. Further studies using frozen tissues
with similar short postmortem acquisition times,
revealed the expression of the high affinity uptake
transporter to be increased in AD cortex as well. When
the ratio of regional uptake activity or expression to
the regional level of choline acetyltransferase was
calculated, the increase in choline transporter activity
and expression was clearly statistically significant.
Further statistical significance in the choline
transporter activity of the AD group was achieved when
the putamen, a region without marked pathology in AD,
was used as an internal standard to control for agonal
state differences in the individual patients
contributing tissue to this study. These increases in
choline transporter expression and activity in AD
indicate disordered regulation of this rate-limiting
component of acetylcholine synthesis above and beyond
that required to compensate for the reduced cholinergic
synaptic availability in AD.
- Language of Publication
- English
- Unique Identifier
- 96187018
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- MeSH Heading (Major)
- Alzheimer Disease|*ME; Brain|*ME; Carrier Proteins|*ME
- MeSH Heading
- Binding, Competitive; Choline|ME; Choline O-Acetyltransferase|ME;
Hemicholinium 3|ME; Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0077-8923
- Country of Publication
- UNITED STATES
Record 7 from database: MEDLINE
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- Title
- Choline. A nutrient that is involved in the regulation
of cell proliferation, cell death, and cell
transformation.
- Author
- Zeisel SH
- Address
- Department of Nutrition, University of North Carolina
at Chapel Hill, School of Public Health 27599-7400, USA.
- Source
- Adv Exp Med Biol, 1996, 399:, 131-41
- Abstract
- Choline deficiency causes hepatocyte proliferation,
apoptosis and transformation. Thus, it is an excellent
model in which to study the molecular mechanisms
underlying these processes. Several interesting
questions can be addressed. What is the first event that
begins the cells on the path towards transformation? Is
it triggered by some autocrine factor produced in
choline depleted cells? Does it involve alteration of
DNA structure with subsequent apoptosis, compensatory
cell proliferation, and enhanced survival of
preneoplastic cells? Is there a specific choline
deficiency signal which triggers apoptosis, with
subsequent compensatory cell proliferation in a
methyl-deficient environment causing hypomethylation of
DNA? Does this result in abnormal transcription of genes
with resulting transformation? Or is the activation of
PKC the first event? PKC-mediated cell proliferation
might then be balanced by down regulation of growth
factor response, withdrawal of which causes apoptosis.
The ensuing high rate of cell turnover might result in
the survival and replication of preneoplastic cells.
Multiple alternative variations of these questions
exist. Whatever the critical first event is, our models
also allow us to ask about molecular differences between
cells that pass through these early events and those
that do not. At first glance, choline deficiency may
seem to be an artificial situation that might rarely
occur in nature. However, the answers to some of the
above questions will help us to understand how changes
in gene expression and the signaling pathways that are
fundamental for many cell functions, might be involved
in liver cell proliferation, death and transformation.
- Language of Publication
- English
- Unique Identifier
- 97091887
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- MeSH Heading (Major)
- Cell Death|*PH; Cell Division|*PH; Cell
Transformation, Neoplastic|*; Choline|*PH; Choline
Deficiency|*CO
- MeSH Heading
- Animal; Cell Line; Human; Models, Biological;
Neoplasms|ET; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0065-2598
- Country of Publication
- UNITED STATES
Record 8 from database: MEDLINE
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- Title
- Choline: an important nutrient in brain development,
liver function and carcinogenesis.
- Author
- Zeisel SH
- Address
- Department of Nutrition, School of Public Health,
University of North Carolina, Chapel Hill 27599.
- Source
- J Am Coll Nutr, 1992 Oct, 11:5, 473-81
- Abstract
- Choline is required to make certain phospholipids
which are essential components of all membranes. It is a
precursor for biosynthesis of the neurotransmitter
acetylcholine and also is an important source of labile
methyl groups. Much attention has been given to the
effect of supplemental choline upon brain function,
i.e., enhancement of acetylcholine synthesis and
release. In addition, choline supplements administered
to rats in utero or shortly after birth permanently
after brain function. The mechanisms for this effect is
unknown and under investigation at this time. Healthy
humans fed diets deficient in choline, and humans fed
parenterally have decreased plasma choline
concentrations and develop liver dysfunction that is
similar to that seen in choline-deficient animals. In
experimental animals, fatty liver occurs in choline
deficiency because phosphatidylcholine synthesis is
required for very low-density lipoprotein secretion.
This accumulation of lipids in liver may explain why
choline-deficient rats spontaneously develop
hepatocarcinoma. We found that choline deficiency was
associated with the accumulation of 1,2-diacylglycerol,
an activator of protein kinase C. Several lines of
evidence indicate that cancers might develop secondary
to abnormalities in protein kinase C-mediated signal
transduction.
- Language of Publication
- English
- Unique Identifier
- 93085083
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- MeSH Heading (Major)
- Brain|*DE/GD; Choline|BL/ME/*PD; Liver|*DE/PH;
Neoplasms|*PC
- MeSH Heading
- Alanine Transaminase|BL; Animal; Diet; Human; Rats;
Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0731-5724
- Country of Publication
- UNITED STATES
Record 9 from database: MEDLINE
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- Title
- CDP-choline: pharmacological and clinical review.
- Author
- Secades JJ; Frontera G
- Address
- F.I.S.A. Medical Department, Barcelona.
- Source
- Methods Find Exp Clin Pharmacol, 1995 Oct, 17 Suppl
B:, 2-54
- Abstract
- Cytidine 5'-diphosphocholine, CDP-choline or
citicoline, is an essential intermediate in the
biosynthetic pathway of the structural phospholipids of
cell membranes, especially in that of
phosphatidylcholine. Upon oral or parenteral
administration, CDP-choline releases its two principle
components, cytidine and choline. When administered
orally, it is absorbed almost completely, and its
bioavailability is approximately the same as when
administered intravenously. Once absorbed, the cytidine
and choline disperse widely throughout the organism,
cross the blood-brain barrier and reach the central
nervous system (CNS), where they are incorporated into
the phospholipid fraction of the membrane and microsomes.
CDP-choline activates the biosynthesis of structural
phospholipids in the neuronal membranes, increases
cerebral metabolism and acts on the levels of various
neurotransmitters. Thus, it has been experimentally
proven that CDP-choline increases noradrenaline and
dopamine levels in the CNS. Due to these pharmacological
activities, CDP-choline has a neuroprotective effect in
situations of hypoxia and ischemia, as well as improved
learning and memory performance in animal models of
brain aging. Furthermore, it has been demonstrated that
CDP-choline restores the activity of mitochondrial
ATPase and of membranal Na+/K+ ATPase, inhibits the
activation of phospholipase A2 and accelerates the
reabsorption of cerebral edema in various experimental
models. CDP-choline is a safe drug, as toxicological
tests have shown; it has no serious effects on the
cholinergic system and it is perfectly tolerated. These
pharmacological characteristics, combined with
CDP-choline's mechanisms of action, suggest that this
drug may be suitable for the treatment of cerebral
vascular disease, head trauma of varying severity and
cognitive disorders of diverse etiology. In studies
carried out on the treatment of patients with head
trauma, CDP-choline accelerated the recovery from
post-traumatic coma and the recuperation of walking
ability, achieved a better final functional result and
reduced the hospital stay of these patients, in addition
to improving the cognitive and memory disturbances which
are observed after a head trauma of lesser severity and
which constitute the disorder known as postconcussion
syndrome. In the treatment of patients with acute
cerebral vascular disease of the ischemic type, CDP-choline
accelerated the recovery of consciousness and motor
deficit, attaining a better final result and
facilitating the rehabilitation of these patients. The
other important use for CDP-choline is in the treatment
of senile cognitive impairment, which is secondary to
degenerative diseases (e.g., Alzheimer's disease) and to
chronic cerebral vascular disease. In patients with
chronic cerebral ischemia, CDP-choline improves scores
on cognitive evaluation scales, while in patients with
senile dementia of the Alzheimer's type, it slows the
disease's evolution. Beneficial neuroendocrine,
neuroimmunomodulatory and neurophysiological effects
have been described. CDP-choline has also been shown to
be effective as co-therapy for Parkinson's disease. No
serious side effects have been found in any of the
groups of patients treated with CDP-choline, which
demonstrates the safety of the treatment.
- Language of Publication
- English
- Unique Identifier
- 96288310
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- MeSH Heading (Major)
- Cytidine Diphosphate Choline|*PD/PK/*TU; Nootropic
Agents|*PD/PK/*TU
- MeSH Heading
- Animal; Biological Availability; Cerebrovascular
Disorders|DT; Dementia|DT; Head Injuries|DT; Human;
Parkinson Disease|DT; Tissue Distribution
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0379-0355
- Country of Publication
- SPAIN
Record 10 from database: MEDLINE
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- Title
- Choline: a conditionally essential nutrient for
humans.
- Address
-
- Source
- Nutr Rev, 1992 Apr, 50:4 ( Pt 1), 112-4
- Abstract
- Tissue concentrations of choline decreased
significantly while serum alanine aminotransferase
activity, a marker of liver injury, increased sharply
(by 50%) when healthy young adult men received a
choline-free semisynthetic diet for three weeks. This
study suggests that choline is an essential nutrient for
humans when excess methionine and folate are not
available in the diet.
- Language of Publication
- English
- Unique Identifier
- 92310714
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- MeSH Heading (Major)
- Choline|*PH; Choline Deficiency|*PP; Liver|*PP
- MeSH Heading
- Alanine Transaminase|BL; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0029-6643
- Country of Publication
- UNITED STATES
Record 11 from database: MEDLINE
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- Title
- Overexpression of choline acetyltransferase
reconstitutes discrete acetylcholine release in some but
not all synapse formation-defective neuroblastoma cells.
- Author
- Zhong ZG; Misawa H; Furuya S; Kimura Y; Noda M;
Yokoyama S; Higashida H
- Address
- Department of Biophysics, Kanazawa University School
of Medicine, Japan.
- Source
- J Physiol Paris, 1995, 89:3, 137-45
- Abstract
- Secretion of acetylcholine (ACh) in neuroblastoma
cells overexpressing choline acetyltransferase (ChAT)
was examined. With transient transfection of ChAT cDNA,
neuroblastoma cells, which have no endogenous ChAT and
either adhere to myotubes or not, failed to form
functional synapses, and thus no evidence for release of
ACh was detected. Stable neuroblastoma cell lines
overexpressing ChAT accumulated ACh inside the cell, and
slowly released ACh to the outside of the cell in a
calcium-independent fashion. However, after co-culturing
them with rat muscle cells, these transformed cells
adhered to myotubes and ACh was secreted in a discrete
fashion into the synaptic cleft efficiently in some
neuroblastoma cell lines but rather inefficiently in
another cell line. The results show that the latent
secretion machinery of ChAT overexpressing neuroblastoma
cells either is competent or possess defect(s) in ACh
release.
- Language of Publication
- English
- Unique Identifier
- 96030107
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- MeSH Heading (Major)
- Acetylcholine|*ME; Choline O-Acetyltransferase|GE/*ME;
Neuroblastoma|PA/*PP; Synapses|*PH
- MeSH Heading
- Animal; Coculture; DNA, Complementary; Human;
Muscles|CY; Transfection; Tumor Cells, Cultured
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0928-4257
- Country of Publication
- FRANCE
Record 12 from database: MEDLINE
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- Title
- Cholinergic synapses in the central nervous system:
studies of the immunocytochemical localization of
choline acetyltransferase.
- Author
- Houser CR
- Address
- Neurology Service, Veterans Administration Medical
Center, West Los Angeles, California 90073.
- Source
- J Electron Microsc Tech, 1990 May, 15:1, 2-19
- Abstract
- Cholinergic synapses can be identified in
immunocytochemical preparations by the use of monoclonal
antibodies and specific antisera to choline
acetyltransferase (ChAT), the synthesizing enzyme for
acetylcholine (ACh) and a specific marker for
cholinergic neurons. Electron microscopic studies
demonstrate that the fibers and varicosities observed in
light microscopic preparations of many brain regions are
small-diameter unmyelinated axons and vesicle-containing
boutons. The labeled boutons generally contain clear
vesicles and one or more mitochondrial profiles. Many of
these boutons form synaptic contacts, and the synapses
are frequently of the symmetric type, displaying thin
postsynaptic densities and relatively short contact
zones. However, ChAT-labeled synapses with asymmetric
junctions are also observed, and their frequency varies
among different brain regions. Unlabeled dendritic
shafts are the most common postsynaptic elements in
virtually all regions examined although other neuronal
elements, including dendritic spines and neuronal somata,
also receive some cholinergic innervation. ChAT-labeled
boutons form synaptic contacts with several different
types of unlabeled neurons within the same brain region.
Such findings are consistent with a generally diffuse
pattern of cholinergic innervation in many parts of the
central nervous system. Despite many similarities in the
characteristics of ChAT-labeled synapses, there appears
to be some heterogeneity in the cholinergic innervation
within as well as among brain regions. Differences are
observed in the sizes of ChAT-immunoreactive boutons,
the types of synaptic contacts, and the predominant
postsynaptic elements. Thus, the cholinergic system
presents interesting challenges for future studies of
the morphological organization and related function of
cholinergic synapses.
- Language of Publication
- English
- Unique Identifier
- 90250513
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- MeSH Heading (Major)
- Central Nervous System|*UL; Choline O-Acetyltransferase|*AN;
Cholinergic Fibers|*UL; Synapses|*UL
- MeSH Heading
- Animal; Cerebral Cortex|UL; Corpus Striatum|UL;
Hippocampus|UL; Human; Immunohistochemistry; Microscopy,
Electron; Spinal Cord|UL; Support, Non-U.S. Gov't;
Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't,
P.H.S.; Thalamus|UL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0741-0581
- Country of Publication
- UNITED STATES
Record 13 from database: MEDLINE
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- Title
- Choline metabolism as a basis for the selective
vulnerability of cholinergic neurons.
- Author
- Wurtman RJ
- Address
- Dept of Brain and Cognitive Sciences, Massachusetts
Institute of Technology, Cambridge 02139.
- Source
- Trends Neurosci, 1992 Apr, 15:4, 117-22
- Abstract
- The unique propensity of cholinergic neurons to use
choline for two purposes--ACh and membrane
phosphatidylcholine synthesis--may contribute to their
selective vulnerability in Alzheimer's disease and other
cholinergic neurodegenerative disorders. When
physiologically active, the neurons use free choline
taken from the 'reservoir' in membrane
phosphatidylcholine to synthesize ACh; this can lead to
an actual decrease in the quantity of membrane per cell.
Alzheimer's disease (but not Down's syndrome, or other
neurodegenerative disorders) is associated with
characteristic neurochemical lesions involving choline
and ethanolamine: brain levels of these compounds are
diminished, while those of glycerophosphocholine and
glycerophosphoethanolamine (breakdown products of their
respective membrane phosphatides) are increased, both in
cholinergic and noncholinergic brain regions. Perhaps
this metabolic disturbance and the tendency of
cholinergic neurons to 'export' choline--in the form of
ACh--underlie the selective vulnerability of the
neurons. Resulting changes in membrane composition could
abnormally expose intramembraneous proteins such as
amyloid precursor protein to proteases.
- Language of Publication
- English
- Unique Identifier
- 92263540
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- MeSH Heading (Major)
- Choline|*ME; Cholinergic Fibers|DE/*ME
- MeSH Heading
- Animal; Human; Nervous System Diseases|ME/PP
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0166-2236
- Country of Publication
- ENGLAND
Record 14 from database: MEDLINE
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- Title
- Citicoline (CDP-choline): mechanisms of action and
effects in ischemic brain injury.
- Author
- DOrlando KJ; Sandage BW Jr
- Address
- Interneuron Pharmaceuticals Inc., Lexington, MA 02173,
USA.
- Source
- Neurol Res, 1995 Aug, 17:4, 281-4
- Abstract
- Citicoline is approved in Europe and Japan for use in
stroke, head trauma and other neurological disorders. It
is presently being evaluated in phase II/III stroke
trials in the United States. Exogenous administration of
CDP-choline provides both choline and cytidine which
access the brain and serve as substrates for the
synthesis of phosphatidylcholine, a primary neuronal
membrane component; the choline also enhances brain
acetylcholine synthesis. Membrane repair and
regeneration is necessary for recovery from stroke.
Furthermore, citicoline may alleviate free fatty
acid-induced toxicity which accompanies ischemic insult.
Data from many pre-clinical and clinical trials support
the hypothesis that citicoline may be a safe and
effective treatment for stroke.
- Language of Publication
- English
- Unique Identifier
- 96000742
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- MeSH Heading (Major)
- Cerebral Ischemia|*DT; Cytidine Diphosphate Choline|*TU
- MeSH Heading
- Animal; Cell Membrane|DE; Clinical Trials; Fatty
Acids, Nonesterified|ME; Human; Membrane Lipids|ME;
Neurons|DE/ME/UL; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0161-6412
- Country of Publication
- ENGLAND
Record 15 from database: MEDLINE
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- Title
- New insight into the biochemical pathology of liver in
choline deficiency.
- Author
- Ghoshal AK
- Address
- Department of Pathology, University of Toronto,
Ontario, Canada.
- Source
- Crit Rev Biochem Mol Biol, 1995, 30:4, 263-73
- Abstract
- A diet deficient in choline can cause liver cancer in
rats. The previous work since 1932 emphasized the
fat-removing ability of choline from the liver. There
are other dietary factors, including methionine, which,
like choline, can remove fat from the liver. These
factors were termed as lipotropes. Since then, choline
deficiency and lipotrope deficiency are used
synonoumously. Recent work since 1980 has clearly
demonstrated that choline deficiency (CD) and lipotrope
deficiency (LD) are not the same. Generation of free
radicals, DNA alterations, liver cell death, and liver
cancer that occur due to CD are not generated by LD.
Generation of free radicals due to CD diet and some of
the agents that counteract free radical action also
prevent CD effects except for lipid accumulation in the
liver. Despite the recent observations on the role of
phospholipase A2 (PLA2) as the protector of the
membranes, it has been found that by preventing the rise
of PLA2 in the liver, cell death can be prevented. These
new findings give choline a distinct role in liver cell
death and cancer rather than the role of lipotrope. A
new hypothesis linking dietary choline deficiency and
liver cancer has been discussed.
- Language of Publication
- English
- Unique Identifier
- 96058539
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- MeSH Heading (Major)
- Choline Deficiency|*ME/PA; Liver|DE/*ME/PA
- MeSH Heading
- Animal; Calcium|PD; Cell Death; Comparative Study;
Diet|AE; Free Radicals|ME; Human; Lipid Peroxidation|DE;
Lipids|ME; Liver Neoplasms|ET; Models, Biological;
Phospholipases A|ME; Rats; Strontium|PD; Support,
Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1040-9238
- Country of Publication
- UNITED STATES
Record 16 from database: MEDLINE
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- Title
- Liver biochemical pathology of choline deficiency and
of methyl group deficiency: a new orientation and
assessment.
- Author
- Ghoshal AK; Farber E
- Address
- Department of Pathology, University of Toronto,
Ontario, Canada.
- Source
- Histol Histopathol, 1995 Apr, 10:2, 457-62
- Abstract
- New information on the pathologic effects of a choline
deficient diet in the rat, in relation to the
biochemical events, has led to a new understanding and
orientation of the pathogenesis of both acute and
chronic consequences in the liver. The biochemical
pathology of choline deficiency is quite different than
that of methyl group (lipotrope) deficiency. These
studies in our laboratory and elsewhere are generating
new insights and hypotheses concerning the genesis of
hepatocyte necrosis and hepatocellular carcinoma in the
rat fed a choline deficient diet.
- Language of Publication
- English
- Unique Identifier
- 95322751
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- MeSH Heading (Major)
- Choline Deficiency|ME/*PA; Lipid Peroxidation|*PH;
Liver|ME/*PA
- MeSH Heading
- Animal; Diet; Human; Methylation; Support, Non-U.S.
Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0213-3911
- Country of Publication
- SPAIN
Record 17 from database: MEDLINE
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- Title
- Metabolism and actions of CDP-choline as an endogenous
compound and administered exogenously as citicoline.
- Author
- Weiss GB
- Address
- M. Hurley & Associates, Inc., Murray Hill, New
Jersey 07974-1584.
- Source
- Life Sci, 1995, 56:9, 637-60
- Abstract
- CDP-choline, supplied exogenously as citicoline, has
beneficial physiological actions on cellular function
that have been extensively studied and characterized in
numerous model systems. As the product of the
rate-limiting step in the synthesis of
phosphatidylcholine from choline, CDP-choline and its
hydrolysis products (cytidine and choline) play
important roles in generation of phospholipids involved
in membrane formation and repair. They also contribute
to such critical metabolic functions as formation of
nucleic acids, proteins, and acetylcholine.
Orally-administered citicoline is hydrolyzed in the
intestine, absorbed rapidly as choline and cytidine,
resynthesized in liver and other tissues, and
subsequently mobilized in CDP-choline synthetic
pathways. Citicoline is efficiently utilized in brain
cells for membrane lipid synthesis where it not only
increases phospholipid synthesis but also inhibits
phospholipid degradation. Exogenously administered
citicoline prevents, reduces, or reverses effects of
ischemia and/or hypoxia in most animal and cellular
models studied, and acts in head trauma models to
decrease and limit nerve cell membrane damage, restore
intracellular regulatory enzyme sensitivity and
function, and limit edema. Thus, considerable
accumulated evidence supports use of citicoline to
enhance membrane maintenance, membrane repair, and
neuronal function in conditions such as ischemic and
traumatic injuries. Beneficial effects of exogenous
citicoline also have been postulated and/or reported in
experimental models for dyskinesia, Parkinson's disease,
cardiovascular disease, aging, Alzheimer's disease,
learning and memory, and cholinergic stimulation.
- Language of Publication
- English
- Unique Identifier
- 95174506
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- MeSH Heading (Major)
- Cytidine Diphosphate Choline|*ME/*PD/PK/TU
- MeSH Heading
- Animal; Anoxia|DT/ME; Cell Membrane|DE/ME; Cells,
Cultured; Head Injuries|DT; Human; Ischemia|DT/ME;
Neurons|DE/PH; Phospholipids|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0024-3205
- Country of Publication
- ENGLAND
Record 18 from database: MEDLINE
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- Title
- Choline acetyltransferase: celebrating its fiftieth
year.
- Author
- Wu D; Hersh LB
- Address
- Department of Biochemistry, University of Kentucky,
Chandler Medical Center, College of Medicine, Lexington
40536-0084.
- Source
- J Neurochem, 1994 May, 62:5, 1653-63
- Abstract
- It is well known that the regulation of choline
acetyltransferase (ChAT) activity under physiological
and pathological conditions is important for the
development and neuronal activities of cholinergic
systems involved in many fundamental brain functions.
This review focuses on recent progress in understanding
the regulation of ChAT at the levels of both the protein
and the mRNA. A deficiency in ChAT activity has been
reported for neurodegenerative conditions such as
Alzheimer's disease, amyotrophic lateral sclerosis, and
schizophrenia. Although a major feature of ChAT
regulation is likely to involve the spatial and temporal
control of transcription, regulation of expression can
also be at the level of RNA processing,
transport/translocation, turnover, or translation. In
addition, there is increasing evidence that ChAT might
be regulated at the posttranslational level by
compartmentation and/or covalent modification, i.e.,
phosphorylation, as well as noncovalent modification
(protein-protein interaction, etc.). Synaptic activity
and the state of neuronal transmission may also involve
the regulation of ChAT at different levels via both
positive and negative feedback loops, as was
demonstrated in the characterization of two ChAT mutant
Drosophila strains. Clearly, identification of
cholinergic-specific elements and the characterization
of the trans-acting factors that bind to them represent
an important area of future research. Equally important
is research on the mechanisms governing ChAT as an
enzymatic entity. The future should be an exciting time
during which we look forward to the elucidation of the
cholinergic signal and its regulation as well as the
determination of the three-dimensional structure of the
enzyme.
- Language of Publication
- English
- Unique Identifier
- 94209870
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- MeSH Heading (Major)
- Brain|*EN; Choline O-Acetyltransferase|BI/DF/*ME
- MeSH Heading
- Alzheimer Disease|EN; Amyotrophic Lateral Sclerosis|EN;
Animal; Cloning, Molecular; Human; Protein Processing,
Post-Translational; RNA, Messenger|ME; Schizophrenia|EN;
Support, U.S. Gov't, P.H.S.; Transcription, Genetic;
Translation, Genetic
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0022-3042
- Country of Publication
- UNITED STATES
Record 19 from database: MEDLINE
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- Title
- Lecithin and choline in human health and disease.
- Author
- Canty DJ; Zeisel SH
- Address
- Department of Nutrition, Food, and Hotel Management at
New York University, NY.
- Source
- Nutr Rev, 1994 Oct, 52:10, 327-39
- Abstract
- Choline is involved in methyl group metabolism and
lipid transport and is a component of a number of
important biological compounds including the membrane
phospholipids lecithin, sphingomyelin, and plasmalogen;
the neurotransmitter acetylcholine; and platelet
activating factor. Although a required nutrient for
several animal species, choline is not currently
designated as essential for humans. However, recent
clinical studies show it to be essential for normal
liver function. Additionally, a large body of evidence
from the fields of molecular and cell biology shows that
certain phospholipids play a critical role in generating
second messengers for cell membrane signal transduction.
This process involves a cascade of reactions that
translate an external cell stimulus such as a hormone or
growth factor into a change in cell transport,
metabolism, growth, function, or gene expression.
Disruptions in phospholipid metabolism can interfere
with this process and may underlie certain disease
states such as cancer and Alzheimer's disease. These
recent findings may be appropriate in the consideration
of choline as an essential nutrient for humans.
- Language of Publication
- English
- Unique Identifier
- 95116033
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- MeSH Heading (Major)
- Choline|ME/*PD; Phosphatidylcholines|CS/ME/*PD
- MeSH Heading
- Animal; Choline Deficiency|ME; Human; Neoplasms|ME;
Nutritional Requirements; Phospholipids|ME; Signal
Transduction; Sphingosine|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0029-6643
- Country of Publication
- UNITED STATES
Record 20 from database: MEDLINE
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- Title
- A review of chemical issues in 1H NMR spectroscopy:
N-acetyl-L-aspartate, creatine and choline.
- Author
- Miller BL
- Address
- UCLA School of Medicine, Harbor-UCLA Medical Center,
Torrance 90509.
- Source
- NMR Biomed, 1991 Apr, 4:2, 47-52
- Abstract
- The structure and function of the chemicals
contributing to the three main peaks seen with 1H NMR
spectroscopy, N-acetyl-L-aspartate (NAA), creatine/phosphocreatine
(Cr), and choline-containing compounds (Cho) is reviewed
and the changes seen with these compounds in various
disease states are briefly outlined. NAA is present
within neurons although its biological function is
largely unknown. NAA is elevated in several degenerative
neurological conditions including amyotrophic lateral
sclerosis and canavan disease, and in high
concentrations it may behave like a neurotoxin. The
creatine peak seen with 1H NMR spectroscopy consists of
creatine and phosphocreatine which serve as a reserve
for high-energy phosphates in the cytosol of muscle and
neurons. They also buffer cellular ATP/ADP. The Cho peak
seen with 1H NMR consists of a complex mixture of Cho-containing
compounds. Cho is a precursor for the neurotransmitter
acetylcholine and for the membrane constituent
phosphatidylcholine. Future studies of changes seen in
the Cho peak with stroke, degenerative dementia, drug
intake, and infectious and neoplastic brain masses will
be of great interest.
- Language of Publication
- English
- Unique Identifier
- 91315964
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- MeSH Heading (Major)
- Aspartic Acid|*AA/CH; Brain Chemistry|*PH;
Choline|*CH; Creatine|*CH
- MeSH Heading
- Human; Nuclear Magnetic Resonance|MT;
Phosphocreatine|CH; Protons; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0952-3480
- Country of Publication
- ENGLAND
Record 21 from database: MEDLINE
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- Title
- Choline and human nutrition.
- Author
- Zeisel SH; Blusztajn JK
- Address
- Department of Nutrition, School of Public Health,
University of North Carolina at Chapel Hill 27599-7400.
- Source
- Annu Rev Nutr, 1994, 14:, 269-96
- Abstract
- Choline is crucial for sustaining life. It modulates
the basic signaling processes within cells, is a
structural element in membranes, and is vital during
critical periods in brain development. Choline
metabolism is closely interrelated with the metabolism
of methionine and folate. We believe that the normal
human diet provides sufficient choline to sustain
healthy organ function. However, vulnerable populations
may become choline deficient, including the growing
infant, the pregnant or lactating woman, the cirrhotic,
and the patient fed intravenously. Further studies of
choline requirements in these groups are required.
- Language of Publication
- English
- Unique Identifier
- 95033449
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- MeSH Heading (Major)
- Choline|*/AD/ME/PH; Nutrition|*
- MeSH Heading
- Animal; Brain|GD/PH; Choline Deficiency; Human;
Neoplasms; Nutritional Requirements; Phospholipids|PH;
Signal Transduction; Support, Non-U.S. Gov't; Support,
U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0199-9885
- Country of Publication
- UNITED STATES
Record 22 from database: MEDLINE
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- Title
- Choline deficiency, lipotrope deficiency and the
development of liver disease including liver cancer: a
new perspective.
- Author
- Ghoshal AK; Farber E
- Address
- Department of Pathology, University of Toronto,
Ontario, Canada.
- Source
- Lab Invest, 1993 Mar, 68:3, 255-60
- Abstract
- Thus, the pathologic consequences of feeding a CD diet
are fatty liver, liver cell death, liver cell
proliferation, and liver cell cancer. The fatty liver
with CD is similar to that with other types of fatty
liver in that the most attractive current hypothesis is
based on some interference with the production and
output of VLDL by the liver. The induction of cell death
appears to be consistent with quite a different
hypothesis, genesis and/or increase in liver free
radicals leading to both acute necrosis and initiation
of carcinogenesis. Especially noteworthy is the low
incidence of liver cirrhosis, even after 2 years of
exposure to the CD diet. The feeding of the CD diet
reproducibly induces severe and persistent fatty liver
coupled with extensive cell death, a combination that is
frequently considered to be appropriate for the
induction of "micronodular" (fatty) cirrhosis
in humans. The findings with the LD diet, the high
incidence of cirrhosis, with severe persistent fatty
liver without significant cell death, together with the
low incidence of cirrhosis with the CD diet, stand out
as unpredictable and strange, according to current
concepts of the pathogenesis of human cirrhosis. The CD
model offers an unusual opportunity to explore in
increasing detail the possible roles of free radicals in
two important problems in pathology and medicine-acute
cell injury and neoplasia. The challenges include
mechanistic studies on how the free radicals are
generated and how they relate to the biological
consequences. The relatively slow sequential changes in
the induction of cell injury and neoplasia makes the CD
model one of the best for mechanistic studies relating
to free radicals.
- Language of Publication
- English
- Unique Identifier
- 93196136
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- MeSH Heading (Major)
- Carcinoma, Hepatocellular|*ET/ME/PP; Choline
Deficiency|*CO/ME/PP; Lipotropic Agents|*ME; Liver
Diseases|*ET/ME/PP; Liver Neoplasms|*ET/ME/PP; Metabolic
Diseases|*CO/ME/PP
- MeSH Heading
- Human; Syndrome
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0023-6837
- Country of Publication
- UNITED STATES
Record 23 from database: MEDLINE
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- Title
- Choline phospholipids: signal transduction and
carcinogenesis.
- Author
- Zeisel SH
- Address
- Department of Nutrition, School of Public Health,
University of North Carolina, Chapel Hill 27599-7400.
- Source
- FASEB J, 1993 Apr, 7:6, 551-7
- Abstract
- Phospholipids act as vital elements in transmembrane
signaling. Agonist-induced hydrolysis of
phosphatidylinositides has been established as a major
mechanism for transmitting messages into the interior of
cells via protein phosphorylation cascades, ultimately
regulating gene transcription. There is a growing body
of evidence that choline phospholipids (phosphatidylcholine,
sphingomyelin, and their metabolites) also are important
mediators and modulators of transmembrane signaling.
These functions may explain how choline phospholipids
influence normal physiological processes as well as a
diverse group of pathological processes.
- Language of Publication
- English
- Unique Identifier
- 93231448
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- MeSH Heading (Major)
- Choline|*ME; Neoplasms|*ET/ME; Phospholipids|*ME;
Signal Transduction|*
- MeSH Heading
- Animal; Human; Protein Kinase C|ME; Support, Non-U.S.
Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0892-6638
- Country of Publication
- UNITED STATES
Record 24 from database: MEDLINE
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- Title
- Choline acetyltransferase.
- Author
- Mautner HG
- Address
-
- Source
- CRC Crit Rev Biochem, 1977 Nov, 4:4, 341-70
- Abstract
- Acetylcholine is essential to neural function. It
synthesis is catalyzed by choline acetyltransferase, the
enzyme responsible for the acetylation of choline by
acetyl coenzye A, a reaction favored slightly
thermodymodynamically and not at all kinetically. An
analytically pure enzyme still has not been obtained;
however, method of purification have been greatly
improved recently. Numerous inhibitors of the enzyme
have been synthesized and their structure-action
relationships examained. Evidence has been accumulated
showing the essential involvement of an imidazole group
in the active site of choline acetyltransferase. The
literature regarding the controversial role to thiol
groups in choline acetyltransferase is reviewed.
Recently, derivatives of coenzyme A have been introduced
as inhibitors of this enzyme and the specificity of
coenzyme A binding has been examined. Possible
mechanisms responsible for the control fo acetylcholine
synthesis are discussed.
- Language of Publication
- English
- Unique Identifier
- 78042632
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- MeSH Heading (Major)
- Choline O-Acetyltransferase|IP/*ME/RE
- MeSH Heading
- Acetylcholine|AA/BI; Acyl Coenzyme A|ME; Animal;
Binding Sites; Brain|EN; Choline|AA; Coenzyme A|ME;
Female; Ganglia|EN; Human; Imidazoles|PD; Kinetics;
Light; Molecular Weight; Placenta|EN; Pregnancy;
Pyridines|PD; Squid; Stereoisomerism; Structure-Activity
Relationship; Sulfhydryl Reagents|PD; Support, U.S.
Gov't, Non-P.H.S.; Thermodynamics; Vinyl Compounds|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0045-6411
- Country of Publication
- UNITED STATES
Record 25 from database: MEDLINE
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- Title
- Uropharmacology: v. choline esters and other
parasympathomimetic drugs.
- Author
- Finkbeiner AE; Bissada NK; Welch LT
- Address
-
- Source
- Urology, 1977 Jul, 10:1, 83-9
- Abstract
- Various parasympathomimetic drugs are discussed,
including the choline esters, bethanechol, carbachol,
methacholine chloride, and furtrethonium. Other
cholinomimetic agents include muscarine, muscarone,
arecholine, and pilocarpine. Anticholinesterase agents
inhibit or inactivate acetylcholinesterase enzyme and
thus result in a prolonged stimulation of cholinergic
receptors by endogenous ACh. Bethanechol is the most
widely used parasympathomimetic drug in the United
States. Its action is mainly muscarinic with activity
largely confined to the urinary bladder and to a lesser
degree the gastrointestinal tract. It can be
administered only subcutaneously or orally, and adequate
dosage is necessary for a successful response.
- Language of Publication
- English
- Unique Identifier
- 77217117
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- MeSH Heading (Major)
- Bladder|*DE; Parasympathomimetics|*PD
- MeSH Heading
- Ammonium Compounds|PD; Animal; Bethanechol
Compounds|AD/AE/PD; Carbachol|PD; Cholinesterase
Inhibitors|PD; Human; Male; Methacholine Compounds|PD;
Muscarine|PD; Muscle, Smooth|DE; Neostigmine|PD;
Phenoxybenzamine|PD; Physostigmine|PD; Pyridinium
Compounds|PD; Urethra|DE
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0090-4295
- Country of Publication
- UNITED STATES
Record 26 from database: MEDLINE
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- Title
- Emerging treatments: replacement therapy with choline
or lecithin in neurological diseases.
- Author
- Barbeau A
- Address
-
- Source
- Can J Neurol Sci, 1978 Feb, 5:1, 157-60
- Abstract
- This review evaluates the theoretical background and
experimental data behind a new development: the
replacement therapy of deficient central cholinergic
systems with the dietary precursors choline or lecithin.
Cholinergic deficiency states are possibly present in
five neurological entities: Huntington's chorea, Tardive
Dyskinesia, Gilles de la Tourette's disease,
Friedreich's ataxia and pre-senile dementia. Preliminary
data from various laboratories, including our own, in
each of these disorders indicate that some clinical
improvement can occasionally be seen, and that this
approach deserves further investigation.
- Language of Publication
- English
- Unique Identifier
- 78166889
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- MeSH Heading (Major)
- Choline|*TU; Nervous System Diseases|*DT;
Phosphatidylcholines|*TU
- MeSH Heading
- Animal; Dyskinesia, Drug-Induced|DT; Friedreich's
Ataxia|DT; Human; Huntington's Disease|DT; Tourette
Syndrome|DT
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0317-1671
- Country of Publication
- CANADA
Record 27 from database: MEDLINE
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- Title
- Effects of consumption of choline and lecithin on
neurological and cardiovascular systems.
- Author
- Wood JL; Allison RG
- Address
-
- Source
- Fed Proc, 1982 Dec, 41:14, 3015-21
- Abstract
- This report concerns possible adverse health effects
and benefits that might result from consumption of large
amounts of choline, lecithin, or phosphatidylcholine.
Indications from preliminary investigations that
administration of choline or lecithin might alleviate
some neurological disturbances, prevent
hypercholesteremia and atherosclerosis, and restore
memory and cognition have resulted in much research and
public interest. Symptoms of tardive dyskinesia and
Alzheimer's disease have been ameliorated in some
patients and varied responses have been observed in the
treatment of Gilles de la Tourette's disease,
Friedreich's ataxia, levodopa-induced dyskinesia, mania,
Huntington's disease, and myasthenic syndrome. Further
clinical trials, especially in conjunction with
cholinergic drugs, are considered worthwhile but will
require sufficient amounts of pure phosphatidylcholine.
The public has access to large amounts of commercial
lecithin. Because high intakes of lecithin or choline
produce acute gastrointestinal distress, sweating,
salivation, and anorexia, it is improbable that
individuals will incur lasting health hazards from
self-administration of either compound. Development of
depression or supersensitivity of dopamine receptors and
disturbance of the cholinergic-dopaminergic-serotinergic
balance is a concern with prolonged, repeated intakes of
large amounts of lecithin.
- Language of Publication
- English
- Unique Identifier
- 83054031
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- MeSH Heading (Major)
- Choline|AE/*TU; Movement Disorders|*DT;
Phosphatidylcholines|AE/*TU
- MeSH Heading
- Acetylcholine|ME; Aging; Atherosclerosis|PC; Diet;
Human; Hypercholesterolemia|PC; Memory; Nervous
System|DE
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0014-9446
- Country of Publication
- UNITED STATES
Record 28 from database: MEDLINE
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- Title
- Molecular biology and neurobiology of choline
acetyltransferase.
- Author
- Salvaterra PM
- Address
- Division of Neurosciences, Beckman Research Institute
of the City of Hope, Duarte, CA 91010.
- Source
- Mol Neurobiol, 1987 Fal, 1:3, 247-80
- Abstract
- In the 45 years since the first description of choline
acetyltransferase (ChAT; EC 2.3.1.6.), significant
progress has been made in characterizing the molecular
properties of this important neurotransmitter synthetic
enzyme. We are now on the verge of understanding its
genetic regulation and biological function(s). The
Drosophila cDNA has been cloned, sequenced, and
expressed in both a eucaryotic and a procaryotic system.
The levels of ChAT specific mRNA have been determined
during Drosophila development. Monoclonal and polyclonal
antibodies have been produced to the enzyme from a
variety of sources and used for biochemical and
immunocytochemical studies. Two well characterized
genetic systems have identified the ChAT gene and
described a series of useful alleles. As a nervous
system specific protein expressed only in the subset of
neurons using acetylcholine as a neurotransmitter, ChAT
is a good model for uncovering the processes and factors
responsible for regulating genes involved in
neurotransmitter phenotype selection and maintenance.
Recent studies have described the purification of a
cholinergic factor from muscle conditioned medium and
indicated the potential importance of nerve growth
factor (NGF) for regulating ChAT expression in the
central nervous system. These factors, or ones remaining
to be discovered, may be involved in the etiology or
disease process of neurodegenerative nervous system
disorders such as Alzheimer's disease.
- Language of Publication
- English
- Unique Identifier
- 90000669
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- MeSH Heading (Major)
- Choline O-Acetyltransferase|*/IM/ME/PH; Neurons|*EN
- MeSH Heading
- Animal; Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0893-7648
- Country of Publication
- UNITED STATES
Record 29 from database: MEDLINE
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- Title
- Choline: an essential dietary nutrient?
- Author
- Sheard NF; Zeisel SH
- Address
- Department of Pediatrics, Harvard Medical School,
Boston, Massachusetts.
- Source
- Nutrition, 1989 Jan, 5:1, 1-5
- Abstract
- Choline (trimethyl-beta-hydroxyethylammonium) is a
quaternary amine which is widely distributed in plants
and animals. It contains three methyl groups which are
important in a number of metabolic reactions, including
the synthesis of methionine and carnitine. Choline is
also a component of the phospholipids
phosphatidylcholine and sphingomyelin, important
constituents of all cell membranes. Finally, choline is
necessary for the synthesis of the neurotransmitter
acetylcholine. Although this compound is considered an
essential nutrient in numerous mammalian species, this
has not been established for humans.
- Language of Publication
- English
- Unique Identifier
- 92199733
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- MeSH Heading (Major)
- Choline|ME/*PH
- MeSH Heading
- Animal; Animal Nutrition; Choline Deficiency|ME;
Human; Nutritional Requirements; Nutritional Status;
Support, Non-U.S. Gov't; Support, U.S. Gov't,
Non-P.H.S.; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0899-9007
- Country of Publication
- UNITED STATES
Record 30 from database: MEDLINE
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- Title
- Phosphatidylcholine as a precursor of choline for
acetylcholine synthesis.
- Author
- Blusztajn JK; Liscovitch M; Mauron C; Richardson UI;
Wurtman RJ
- Address
- Department of Brain and Cognitive Sciences,
Massachusetts Institute of Technology, Cambridge.
- Source
- J Neural Transm Suppl, 1987, 24:, 247-59
- Abstract
- It has been hypothesized that the selective
vulnerability of certain brain cholinergic neurons in
Alzheimer's disease may reflect the unique way that
choline is utilized by these neurons, i.e. not only as a
component of major membrane phospholipids, e.g.
phosphatidylcholine (PC), but also as a precursor of
their neurotransmitter, acetylcholine (ACh). A prolonged
utilization of choline liberated from PC, for ACh
production, without adequate resynthesis of this lipid,
might result in a net loss of the phosphatide followed
by an impairment of membrane function and loss of
cellular viability. Studies described in this paper,
performed on electrically stimulated striatal slices and
on cholinergic cell lines, test this hypothesis. 1)
Electrically-stimulated striatal slices continue to
release ACh, and sustain their free choline and ACh
levels, even when perfused with a choline-free medium.
Striatal levels of PC decline under these circumstances,
and this decline can be blocked by adding tetrodotoxin
(which blocks neuronal depolarization) or choline to the
medium. The other major membrane phospholipids,
phosphatidylserine and phosphatidylethanolamine, also
decline proportionately to PC when slices are stimulated
in the absence of choline. 2) In a population of purely
cholinergic cells (human neuroblastoma, LA-N-2), ACh can
be synthesized from choline derived from degradation of
endogenous PC formed de novo by methylation of
phosphatidylethanolamine. 3) PC content of cells in
culture (neuroblastoma X glioma hybrid, NG 108-15) can
be altered by adding various amounts of choline to the
growth media. The proportion of PC in the cells
apparently affects cellular survival and rate of growth.
Taken together these data demonstrate that cholinergic
neurons utilize the choline stored in PC to synthesize
ACh; that this process may lead to a depletion in
membrane phospholipids (when choline supply is
inadequate); and that the resulting changes in neuronal
membrane composition might adversely affect cellular
viability.
- Language of Publication
- English
- Unique Identifier
- 88061316
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- MeSH Heading (Major)
- Acetylcholine|*BI; Choline|*ME; Phosphatidylcholines|*ME;
Receptors, Cholinergic|*ME
- MeSH Heading
- Animal; Corpus Striatum|ME; Human; In Vitro;
Phospholipids|ME; Rats; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0303-6995
- Country of Publication
- AUSTRIA
Record 31 from database: MEDLINE
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- Title
- Hepatotoxicity associated with choline magnesium
trisalicylate: case report and review of salicylate-induced
hepatotoxicity.
- Author
- Cersosimo RJ; Matthews SJ
- Address
-
- Source
- Drug Intell Clin Pharm, 1987 Jul, 21:7-8, 621-5
- Abstract
- A case of a 21-year-old woman who had developed mild
hepatotoxicity while receiving choline magnesium
trisalicylate therapy is described. She presented with
fever and mild hepatic enzyme elevations before
salicylate therapy was instituted. Liver function tests
(LFT) returned to normal within five days of
hospitalization but she continued to develop daily
fevers. Blood, urine, and throat cultures were negative.
An acute viral illness or reactivation of systemic lupus
erythematosus were the suspected diagnoses. Choline
magnesium trisalicylate was then administered in an
effort to control her fever, and was successful. After
three days of salicylate therapy her LFT values began to
rise. They continued to rise for five more days before
salicylate hepatotoxicity was suspected. Choline
magnesium trisalicylate was discontinued after eight
days and the patient's LFT quickly returned to normal.
The source of fever was never identified, although
infection with cytomegalovirus was considered the most
likely cause. Salicylate-induced hepatotoxicity is
reviewed.
- Language of Publication
- English
- Unique Identifier
- 87275455
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- MeSH Heading (Major)
- Anti-Inflammatory Agents, Non-Steroidal|*AE/TU;
Choline|*AA/AE/TU; Hepatitis, Toxic|*ET; Liver|*DE;
Salicylates|*AE/TU
- MeSH Heading
- Adult; Case Report; Female; Fever of Unknown Origin|DT;
Human
ô
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0012-6578
- Country of Publication
- UNITED STATES
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