Some effects of folate deficiency on mentals status in street dwelling homeless mentally ill (original) (raw)
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Neurochemistry and Neuroendocrinology of Schizophrenia: A Selective Review
Schizophrenia Bulletin, 1993
Neurochemical investigation has played a major role in the search for the cause of schizophrenia. Initial research strategies involved the direct measurement of neurochemical substances in biological fluids. Subsequently, indirect measures of brain biochemistry including pituitary hormones and responses to pharmacologic probes were examined. Recent advances in in vivo functional neuroimaging, biochemical neuropathology, and molecular genetics have extended the scope of clinical neurochemical studies. The historical emphasis on the dopamine neurotransmitter system has subsided in the wake of the demonstrated limitations of the dopamine hypothesis of schizophrenia and increased evidence for the role of other neurotransmitters in the pathophysiology of schizophrenia as well as their interactions with dopamine neural systems. The neurorransmitters that have come under increasing scrutiny include serotonin, norepinephrine, glutamate, and related excitatory amino acids, and the neuropeptides cholecystokinin and neurotensin. In this article, the authors reviewed significant recently published neurochemical and neuroendocrine studies of schizophrenia in the context of previous work and found an extensive but fragmentary body of data which provides neither consistent nor conclusive evidence for any specific etiologic theory. Aspects of the disease and methodological limitations that may account for this as well as future research strategies are discussed. I 3J m 2 CD C |-m z by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from ID CO CO by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from m CD c I-rm by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from m CD c I-m by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from CO CO CO CO oo by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from m z CD rr-m z by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from CD CO CO CO CO y by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from CO CO CO by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from Discussion The extensive data produced by by guest on September 16, 2016 http://schizophreniabulletin.oxfordjournals.org/ Downloaded from Chang, W.; Chen, T.; Lee, C; Hung, J.; Hu, W.; and Yeh, E. Plasma homovanillic acid levels and subtyping of schizophrenia. by guest on September 16, 2016
Schizophrenia Research, 2009
The role of fibroblast growth factor receptors (FGFR) in normal brain development has been welldocumented in transgenic and knock-out mouse models. Changes in FGF and its receptors have also been observed in schizophrenia and related developmental disorders. The current study examines a transgenic th(tk-)/th(tk-) mouse model with FGF receptor signaling disruption targeted to dopamine (DA) neurons, resulting in neurodevelopmental, anatomical, and biochemical alterations similar to those observed in human schizophrenia. We show in th(tk-)/ th(tk-) mice that hypoplastic development of DA systems induces serotonergic hyperinnervation of midbrain DA nuclei, demonstrating the co-developmental relationship between DA and 5-HT systems. Behaviorally, th(tk-)/th(tk-) mice displayed impaired sensory gaiting and reduced social interactions correctable by atypical antipsychotics (AAPD) and a specific 5-HT2A antagonist, M100907. The adult onset of neurochemical and behavioral deficits was consistent with the postpubertal time course of psychotic symptoms in schizophrenia and related disorders. The spectrum of abnormalities observed in th(tk-)/th(tk-) mice and the ability of AAPD to correct the behavioral deficits consistent with human psychosis suggests that midbrain 5-HT2A-controlling systems are important loci of therapeutic action. These results may provide further insight into the complex multi-neurotransmitter etiology of neurodevelopmental diseases such autism, bipolar disorder, Asperger's Syndrome and schizophrenia.
Schizophrenia-associated neural growth factors in peripheral blood. A review
European Neuropsychopharmacology, 2006
In this paper we review the findings on neural growth factors in the peripheral blood of schizophrenia patients. The studies we review provide evidence for the fact that in schizophrenia the levels of growth factors in peripheral blood are disturbed. The most robust results (7 studies) are reported for S100B protein, which seems to be elevated in acute psychosis and in patients with predominant negative symptoms. We conclude that there are aberrant levels of growth factors in peripheral blood in schizophrenia patients, probably most notably in patients with negative symptoms. Large-scale longitudinal multivariate studies, investigating the levels of several growth factors at the same time might give insight in etiological processes and identify clinically useful subsets of patients within the heterogeneous schizophrenia sample. D
Current Perspectives on the Pathophysiology of Schizophrenia, Depression, and Anxiety Disorders
Medical Clinics of North America, 2001
In the 1990s, significant advances in basic and clinical neuroscience yielded new perspectives on the neurobiology and treatment of major psychiatric disorders. Insights into the pathophysiology of psychiatric disorders have been associated with the introduction of new medication classes, such as the atypical neuroleptics or serotonin reuptake inhibitors, that largely have supplanted older pharmacotherapies that had poorer efficacy or tolerability. This article reviews advances in the neurobiology of three major psychiatric disorders: schizophrenia, major depressive disorder, and panic disorder. These three disorders have been the focus Supported by NIAAA (KO2 AA 00261-01) and the Department of Veterans Affairs 559 560 KRYSTAL et a1 of a great deal of research, and advances in the current understanding of their neurobiology have occurred. Schizophrenia, major depression, and panic disorder illustrate the classes of thought disorder, affective disorder, and anxiety disorder. The phenomenology and neurobiology of each disorder are introduced briefly. Although the genetics of these disorders are not clear, progress in this area also is addressed, when relevant. The relevance of the current understanding of the neurobiology of each disorder for treatment is considered briefly. Interested readers seeking an introduction of greater depth are referred to reviews on these SCHIZOPHRENIA Schizophrenia is a profoundly disabling chronic illness with insidious onset in adolescence or early adulthood, variable course, and a growing array of treatment^.^^ Signs and symptoms of this disorder include hallucinations and delusions and encompass many aspects of cognitive and emotional function. Schizophrenia frequently produces social isolation and vocational impairment. In 1990, the economic burden of schizophrenia was greater than $30 million, and it exceeded the economic impact of cancer.lo6 Genetic, neurochemical, and neural circuitry insights into the neurobiology of this disorder are highlighted in this section.
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Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatically that a biochemical like tryptamine, for example, is converted into the hallucinogen dimethyltryptamine. Central to endogenous methylation activity is the folate cycle, which generates the primary transferable methyl groups in mammalian biochemistry. The relevance of this cycle to mental health becomes clear when the cycle is dysregulated, often leading to a buildup of both homocysteine and S-adenosylhomocysteine (SAH), while accompanied by a transient reduction in the intended physiologic target, S-adenosylmethionine (SAM). This paper includes an in-depth review of the causes of folate cycle perturbations associated with psychotic symptoms, expounding on alternative downstream pathways which are activated and pointing toward potential etiologic agents of the associated psychosis, the methylated tertiary amines N-methylsalsolinol, N-methyl-norsalsolinol, and adrenochrome, which appear in scientific reports concerning their association with hallucinogenic and/or neurotoxic outcomes. Electrotopological state (E-state) data has been generated for these compounds, illustrating a strong similarity with hallucinogens, particularly in terms of the Estate of the nitrogen in their tertiary amine moieties. In light of the role the folate cycle plays in transmethylation, neuroprotective strategies to prevent the transition to psychosis are suggested, including the advisory that folate supplementation can be harmful depending on the status of other relevant biochemicals.
Reduced cerebrospinal fluid and plasma nerve growth factor in drug-naïve psychotic patients
Schizophrenia Research, 2009
Impaired expression and function of several major neurotrophic factors such as nerve growth factor (NGF) has been proposed to contribute to the neurodevelopmental pathology of schizophrenia. However, the evidence in the majority of studies is based on variable and inconsistent levels of plasma NGF in diverse populations of early psychosis or medicated patients with chronic schizophrenia. We report here the first study comparing NGF levels in cerebrospinal fluid (CSF) and plasma from a unique patient cohort (unmedicated, early psychotic patients with similar racial and dietary patterns) and matched healthy controls. Significantly lower levels of NGF in both CSF (p = 0.038) and plasma (p = 0.002) were observed in drug-naïve first-episode psychosis patients as compared to controls. The levels of NGF in the CSF correlated (p = 0.05) to the plasma values in controls. The data on plasma NGF confirm the reported deficits of NGF in drug-naïve first-episode psychosis. The reduced levels first time observed here may have important implications to repeatedly reported neurobiological and clinical deficits which are discussed.
Psychoneuroendocrinology of Schizophrenia
Psychiatric Clinics of North America, 1998
The study of the psychoneuroendocrinology of schizophrenia has yielded an extensive but inconclusive body of data. Investigations to date have been limited by several factors, including the confounding effects of neuroleptic drugs, methodologic limitations, and lack of appreciation for the heterogeneity of the illness. Previously, the focus of research has been on the measurement of anterior pituitary hormones. This has been guided by the assumptions that these hormones are regulated by the central nervous system (CNS) to a significant degree13, 39 and that the unique anatomic relationship of the pituitary gland to the hypothalamus and CNS is potentially relevant. The indirect measurement of the neurochemical activity of particular brain structures involved in pituitary hormone regulation by use of pharmacologic probes and neurotransmitter agonists or antagonists has been helpful in the attempt to determine the specific anatomic level of hormonal regulation (pituitary, hypothalamic, or suprahypothalamic). Results have been relatively modest in scope, however, and few unequivocal pathophysiologic findings have been discovered so far. Previous reviews have essentially rounded up the usual suspects in terms of anterior pituitary and adrenal hormones examined in traditional paradigms (i.e., measuring basal levels, 24-hour secretion, responses to pharmacologic challenges). This review proceeds similarly, but it also explores other promising areas of research, including the posterior pituitary hormones and the potential impact of gonadal hormones such as estrogen and progesterone on the pathophysiology of schizophrenia. The neurobiologic basis for the pronounced gender differences observed in schizophrenia and the possible gonadal hormone contributions to these effects have yet to be investigated fully, but initial preclinical and clinical results merit careful examination.