Concentrations of β‐Phenylethylamine in Plasma and Plateletes of Schizophrenics

Abstract

The plasma and platebet PEA levels of 20 normal subjects and 17 schizophrenic patients were investigated using a high‐performance liquid chromatography. In the normals the mean plasma and platelet levels of PEA were 4.9 ± 1.9 ng/ml and 1.78 ± 1.01 ng/mg protein, respctively, while in the schizophrenics, those were 12.1 ± 7.9 ng/ml and 0.77 ± 0.5 ng/mg protein, respectively. The plasma PEA levels of the schizophrenics were significantly higher than those of the normals, and the platelet PEA levels of the schizophrenics were lower than those of the normals.

Credneramides A and B: Neuromodulatory Phenethylamine and Isopentylamine Derivatives of a Vinyl Chloride-Containing Fatty Acid from cf. Trichodesmium sp. nov.

“…28,29 This class of compounds has also been implicated in the pathogenesis of several neurologic diseases including depression, attention deficit and hyperactivity disorder (ADHD), and schizophrenia. 28,29,32 Given the substantial evidence of neuromodulation by phenethylamines, the neuromodulatory effects of credneramide A ( 1 ) are reasonable.…”

“…Fatty acids with phenethylamine have been encountered increasingly among cyanobacterial metabolites. PEA derivatives have a well-recognized role in mammalian physiology as an endogenous neurotransmitter that has been shown to bind trace amine (TAAR), dopaminergic, and GABA receptors. − By binding to these receptors, PEA derivatives modulate higher cognitive function via a capacity to act as hallucinogens, stimulants, and antidepressants. , This class of compounds has also been implicated in the pathogenesis of several neurologic diseases including depression, attention deficit and hyperactivity disorder (ADHD), and schizophrenia. ,, Given the substantial evidence of neuromodulation by phenethylamines, the neuromodulatory effects of credneramide A ( 1 ) are reasonable.…”

Trace amine-associated receptor 1—Family archetype or iconoclast?

“…The results from these studies, often but not always replicated (Anderson et al, 1984), correlated levels of PEA, TYR, TRYP, or their metabolites in blood and/or urine with methylphenidate and AMPH exposure (Borison et al, 1975), hypertension (Andrew et al, 1993), and hepatic encephalopathy (Manghani et al, 1975) as well as mental conditions including schizophrenia (Boulton et al, 1967;Vogel, 1967;Faurbye, 1968;Zeller et al, 1976;Sandler & Reynolds, 1976;Boulton, 1980;Boulton, 1982;Szymnanski et al, 1987;Myojin et al, 1989;O'Reilly et al, 1991;O'Reilly & Davis, 1994;Buckland et al, 1997), Tourette's syndrome (Baker et al, 1993), attention deficit hyperactivity disorder (i.e. ADHD; Baker et al 1991;Kusaga, 2002), migraine (Hannington, 1967;Smith et al, 1970;Sever, 1979;D'Andrea et al, 2003b) and other headache Aridon et al, 2004), and depression Reynolds, 1979;Sandler et al, 1980;Chance et al, 1985;Davis & Boulton, 1994).…”

Novel association approach for determining the genetic predisposition to schizophrenia: Case‐control resource and testing of a candidate gene

“…Elevated plasma or urinary levels of PEA have been observed in schizophrenic patients [Fischer et al, 1972;Potkin et al, 1979Potkin et al, , 1980Jeste et al, 1980;Yoshimoto et al, 1987;Myojin et al, 1989;O'Reilly et al, 19911, but two studies did not show differences [Schweitzer et al, 1975;Szymanski et al, 19871. Reports of significantly higher PEA levels in schizophrenics than controls do not appear to be confounded by age [Jeste et al, 1980;Myojin et al, 1989;O'Reilly et al, 19911, sex [Myojin et al, 1989;O'Reilly et al, 19911, diet [OReilly et al, 19911, and medication status or dosage [Potkin et al, 1979;Yoshimoto et al, 1987;Myojin et al, 1989;O'Reilly et al, 19911. The structure of PEA is nearly identical to amphetamine (alpha-methyl PEA), an abused drug that induces a paranoid psychosis that mimics some forms of schizophrenia.…”