Plasma phenylethylamine in schizophrenic patients
References (26)
- et al.
Simultaneous analysis of twelve biogenic amine metabolites in plasma, cerebrospinal fluid and urine by capillary column gas chromatography-high resolution mass spectrometry with selected ion monitoring
J Chromatogr
(1986) - et al.
Phenylacetic acid in CSF and serum of Indian schizophrenic patients
Progr Neuro-Psychopharmacol Biol Psychiatry
(1991) - et al.
A probable neuroleptic effect on platelet monoamine oxidase in chronic schizophrenic patients
Psychiatry Res
(1981) - et al.
‘Mini-mental stage’: A practical method for grading the cognitive state of patients for the clinician
J Psychiatr Res
(1975) - et al.
B-Phenylethylamine enhances single cortical neurone responses to noradrenalin in the rat
Brain Res Bull
(1988) - et al.
Plasma phenylethylamine and phenylalanine in chronic schizophrenic patients
Biol Psychiatry
(1987) - et al.
Urinary excretion and platelet monoamine oxidase activity in schizophrenia
Psychiatry Res
(1987) The Scale for the Assessment of Negative Symptoms (SANS)
(1983)The Scale for the Assessment of Positive Symptoms (SAPS)
(1984)
Phenylethylamine and phenylacetic acid in CSF of schizophrenics and healthy controls
Arch Psychiatr Nervenkr
Cerebral aryl alkyl aminergic mechanisms
Phenylethylamine in the CNS: Effects of monoamine oxidase inhibiting drugs, deuterium substitution and lesions and its role in the neuromodulation of catecholaminergic neurotransmission
J Neural Transm [Suppl]
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Biogenic amines and the winemaking process
2021, Managing Wine Quality: Volume 2: Oenology and Wine Quality<sup>13</sup> C-phenylalanine breath test and serum biopterin in schizophrenia, bipolar disorder and major depressive disorder
2018, Journal of Psychiatric ResearchCitation Excerpt :Urinary phenylalanine was identified as one of 20 differential metabolites responsible for the discrimination between major depressive disorder (MDD) and bipolar disorder (BPD) subjects (Chen et al., 2015). Regarding metabolites of phenylalanine, plasma phenylethylamine, an endogenous neuroamine, was significantly higher in patients with schizophrenia (Janssen et al., 1999; O'Reilly et al., 1991), and plasma or urinary phenylacetic acid, a main metabolite of phenylethylamine, was significantly lower in patients with MDD (Sabelli et al., 1986) and BPD (Sabelli et al., 1983) than in controls. Plasma biopterin level, which reflects BH4 level (Fiege et al., 2004; Richardson et al., 2005), was decreased in patients with schizophrenia and schizoaffective disorder compared to that in controls (Richardson et al., 2005, 2007), although a few studies reported no significant differences in urine or CSF samples (Duch et al., 1984; Garbutt et al., 1982).
Trace Amines in Neuropsychiatric Disorders
2016, Trace Amines and Neurological Disorders: Potential Mechanisms and Risk FactorsA genetic locus in 7p12.2 associated with treatment resistant schizophrenia
2014, Schizophrenia ResearchCitation Excerpt :DDC, also known as aromatic l-amino acid decarboxylase (AADC), catalyzes the decarboxylation of l-3,4-dihydroxyphenylalanine (DOPA) to dopamine (DA), l-5-hydroxytryptophan to serotonin (5-HT), and l-tryptophan to tryptamine. There is extensive information relating DDC to schizophrenia (Davis et al., 1991; O'Reilly et al., 1991; Reith et al., 1994; Borglum et al., 2001; Grunder et al., 2003; Ikemoto et al., 2003). Expression data of DDC or GRB10 for the three genotypes of rs2237457 or rs2329487 are plotted as a function of age in Fig. 3.
Behavioral outcomes of monoamine oxidase deficiency: Preclinical and clinical evidence
2011, International Review of NeurobiologyCitation Excerpt :The main MAO‐B substrate, PEA, is widely regarded as an endogenous amphetamine, in view of its similar chemical structure and effects in vivo, which include increased alertness, euphoria, insomnia, and tremor (Baud et al., 1985; Zucchi et al., 2006). In line with this concept, numerous studies have highlighted a key role of this trace amine in the pathophysiology of schizophrenia and other neuropsychiatric disorders (Beckmann et al., 1983; Szymanski et al., 1987; O'Reilly et al., 1991; Berry, 2007). Alterations of MAO‐B activity and expression have been associated with a broad constellation of neuropsychiatric manifestations, including psychotic disorders, depression, alcoholism, impulsivity, and neurodegenerative diseases (Mann and Chiu, 1978; Adolfsson et al., 1980; Sandler et al., 1993).
Trace amine-associated receptor 1-Family archetype or iconoclast?
2007, Pharmacology and Therapeutics
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We wish to thank G. Stegeman and H. Miyashita for expert technical assistance and the Friends of Schizophrenia, Saskatchewan Health, and the Medical Research Council of Canada for financial support