Abstract: This invention provides methods of increasing or enhancing the synthesis and levels of phospholipids, synapses, synaptic proteins, and synaptic membranes by a neural cell or brain cell; methods of treating a subject with a memory disorder, memory impairment, neurological disorder, or brain disease or disorder, comprising administering to the subject a composition comprising an omega-3 fatty acid, an omega-6 fatty acid, uridine, a metabolic precursor thereof, or a combination thereof.

Abstract: This invention provides methods of enhancing brain development; increasing or enhancing intelligence; increasing or enhancing synthesis and levels of phospholipids, synapses, synaptic proteins, and synaptic membranes by a neural cell or brain cell, comprising contacting a subject or a pregnant or nursing mother thereof with a composition comprising an omega-3 fatty acid, an omega-6 fatty acid, and/or uridine, a metabolic precursor thereof, or a combination thereof.

Abstract: The present invention provides methods for increasing secretion of dopamine and other neurotransmitters and treating or reducing the incidence of diseases involving decreased secretion of dopamine and other neurotransmitters, e.g. Parkinson's disease, comprising administering to the subject a uridine or a source thereof, and compositions for treating or reducing an incidence of Parkinson's disease, comprising a uridine, a uridine monophosphate, or a source thereof.

Abstract: The present invention provides methods of stimulating or enhancing production of a cellular membrane, improving a cognitive function or a neurological function, treating or ameliorating a decline in a cognitive function or a neurological function, increasing cytidine levels, or treating a neurological disorder in a subject, comprising administering a uridine, a uridine precursor, or a derivative or metabolite thereof to the subject. The invention also provides methods of improving neural function, comprising contacting the neuron with a uridine, a uridine precursor, or a derivative or metabolite thereof.

Abstract: The present invention provides methods of improving a cognitive function or a neurological function, treating or ameliorating a decline in a cognitive function or a neurological function, increasing cytidine levels, or treating a neurological disorder in a subject, comprising administering a uridine, a uridine precursor, or a derivative or metabolite thereof to the subject. The invention also provides methods of improving neural function, comprising contacting the neuron with a uridine, a uridine precursor, or a derivative or metabolite thereof.

Abstract: This invention provides methods of increasing or enhancing the synthesis and levels of phospholipids, synapses, synaptic proteins, and synaptic membranes by a neural cell or brain cell; methods of treating a subject with a memory disorder, memory impairment, neurological disorder, or brain disease or disorder, comprising administering to the subject a composition comprising an omega-3 fatty acid, an omega-6 fatty acid, uridine, a metabolic precursor thereof, or a combination thereof.

Abstract: This invention provides methods of enhancing brain development; increasing or enhancing intelligence; increasing or enhancing synthesis and levels of phospholipids, synapses, synaptic proteins, and synaptic membranes by a neural cell or brain cell, comprising contacting a subject or a pregnant or nursing mother thereof with a composition comprising an omega-3 fatty acid, an omega-6 fatty acid, and/or uridine, a metabolic precursor thereof, or a combination thereof.

Abstract: The present invention provides methods of increasing the level or release of gamma aminobutyric acid (GABA) in the brain, treating Alzheimer's disease, Huntington's disease, symptoms thereof, anxiety, aggression, insomnia, cognitive or memory disturbances; seizures of any cause (e.g. idiopathic epilepsy), primary or metastatic brain tumors, depression (e.g. bipolar depression), or pain (e.g. neuropathic pain), comprising administration of glutamine, a salt thereof, or a glutamine-rich peptide. The present invention also provides methods for decreasing the level or release of GABA in the brain and treating hepatic encephalopathy, depressed consciousness, and coma, comprising decreasing dietary intake of glutamine.

Abstract: Compositions and methods of losing weight are described that are suitable for individuals susceptible to gastric hyperacidity or gastroesophageal reflux. The compositions include in part a snack food having two or more rapidly digestible carbohydrates, in which the foodstuff or an aqueous mixture of the foodstuff and water has a pH equal to or greater than about 6, and in which the snack is substantially protein-free. The method of weight loss suitable for an individual with gastric hyperacidity includes substantially limiting the individual's caloric intake to about 1400 calories or less for women and 1800 calories or less for men in which the caloric intake includes one or more substantially protein-free snack foodstuffs having two or more rapidly digestible carbohydrates, in which an aqueous mixture of the foodstuff with water has a pH equal to or greater than about 6 and in which the individual loses weight.

Abstract: Methods of treating certain neurological diseases using exogenous uridine or a uridine source alone as a precursor of endogenous cytidine, particularly in the human brain, are disclosed. Methods are also disclosed wherein exogenous uridine or a uridine source is combined either with drugs increasing uridine availability or with compounds that serve as a source of choline in phospholipid synthesis.

Abstract: Antagonists to platelet-activating factor provide analgesic effects as well as limit the release of inflammatory mediators. Use of these antagonists in the form of pharmaceutical compositions or nutritionals is beneficial (1) in the treatment of acute and/or chronic pain; (2) in the inhibition of inappropriate or excessive contraction of the uterus; (3) in the treatment of septic shock; and (4) in the inhibition of angiogenesis and/or tumor cell proliferation.

Abstract: This invention relates to compositions and methods for preventing and treating cognitive dysfunction or memory impairment. The compositions include an effective amount of citicoline, or pharmaceutically-acceptable salts thereof, and one or more of the compounds selected from the group consisting of linoleic acid and linolenic acid. Other compositions of this invention include an effective amount of citicoline, or pharmaceutically-acceptable salt thereof, wherein said citicoline is metabolized to form at least one of cytidine, uridine, and choline. Still other compositions of this invention include effective amounts of choline, cytidine, and/or uridine, or their pharmaceutically-acceptable salts. This invention also encompasses methods for preparing these compositions.

Abstract: A method of treating stress in a patient showing stress related symptoms is disclosed, where the method comprises administering to the patient an effective amount of a serotoninergic drug or prodrug. Specific examples of such drugs are described, and include, among others, tryptophan or 5-hydroxytryptophan, or their salts.

Abstract: Compositions and methods of losing weight are described that are suitable for individuals susceptible to gastric hyperacidity or gastroesophageal reflux. The compositions include in part a snack food having two or more rapidly digestible carbohydrates, in which the foodstuff or an aqueous mixture of the foodstuff and water has a pH equal to or greater than about 6, and in which the snack is substantially protein-free. The method of weight loss suitable for an individual with gastric hyperacidity includes substantially limiting the individual's caloric intake to about 1400 calories or less for women and 1800 calories or less for men in which the caloric intake includes one or more substantially protein-free snack foodstuffs having two or more rapidly digestible carbohydrates, in which an aqueous mixture of the foodstuff with water has a pH equal to or greater than about 6 and in which the individual loses weight.

Abstract: A method of treating Mild Cognitive Impairment has been discovered. The treatment method comprises administering an effective amount of a serotonergic agent, including, but not limited to dexnorfenfluramine. The agent can be any serotonergic agonist, partial agonist, serotonin reuptake inhibitor, or combinations of these agents. The treatment method also encompasses combinations of serotonergic agents and non-steroidal anti-inflammatory agents. The treatment method may also delay the onset of Mild Cognitive Impairment, dementia, or both.

Abstract: A method of treating Mild Cognitive Impairment (MCI) has been discovered. The treatment includes administering an effective amount of a natural product that increases soluble amyloid precursor protein (APPs) expression. Examples of a natural product suitable for the method include, but are not limited to, resveratrol, capsaisin, olvanil, resiniferatoxin, arvanil, linvanil, capsazepine, or combinations of these naturally occurring substances. The treatment can also be used to prevent or alleviate the dementia, or to delay its onset. Moreover, a foodstuff is disclosed that incorporates a natural product useful in treating MCI.

Abstract: It has been discovered that the stimulation of &bgr;-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising &bgr;-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by &bgr;-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of &bgr;-adrenergic receptors.

Abstract: It has been discovered that the stimulation of &bgr;-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising &bgr;-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by &bgr;-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of &bgr;-adrenergic receptors.

Abstract: Methods of treating certain neurological diseases using exogenous uridine or a uridine source alone as a precursor of endogenous cytidine, particularly in the human brain, are disclosed. Methods are also disclosed wherein exogenous uridine or a uridine source is combined either with drugs increasing uridine availability or with compounds that serve as a source of choline in phospholipid synthesis.

Abstract: It has been discovered that lipophilic hormones that interact with cytosolic or nuclear receptors regulate APP expression and synthesis, through modification of APP mRNA stability and/or regulation of APP gene transcription and translation activities. These studies demonstrate that the treatment of brain cells with estrone or 17&bgr;-estradiol results in a reduction in the level of APP holoprotein expression, without a concomitant change in the total level of cell protein. The reduction in the level of APP holoprotein caused by estrone or 17&bgr;-estradiol is also expected to reduce the production of neurotoxic APP fragments. In as much as estrogen deficiency in postmenopausal women is associated with a higher incidence of Alzheimer's disease, this discovery opens the possibility that estrogen therapy may prevent some of the neurodegenerative and cognitive changes associated with Alzheimer's disease, aging and other disease conditions associated with such neurodegenerative and cognitive decline.