Platelet monoamine oxidase activity and deficit syndrome schizophrenia

Samson, Jacky; Gurrera, Ronald J.; Nisenson, Laura G.; Schildkraut, Joseph J.

doi:10.1016/0165-1781(94)02555-w

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…The enzyme preferentially degrades benzylamine and phenylethylamine and targets a wide variety of specific neurotransmitters involved in the primary substrates of MAO in the brain, including epinephrine (EP), norepinephrine (NE), dopamine (DA), serotonin (5-HT), and β-phenylethylamine (PEA) (1,2). The unique position of MAO in modulating the function of a diverse series of specific neurotransmitters in association with various conditions, including mood disorders (3), anxiety and depression (4,5), schizophrenia (6), attention deficit hyperactivity disorder (7)(8)(9), migraine (10), sexual maturation (11) and neurodegenerative diseases (12), has attracted significant attention to the protein as a therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

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Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

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Section: Introductionmentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

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“…These authors proposed a new way of subdividing negative symptoms into primary or "deficit" symptoms and secondary negative symptoms, considering the former to be direct expressions of schizophrenic pathology and the latter to relate to other features accompanying the illness (10). Subsequently, Samson et al reported differences between subgroups of schizophrenic subjects in platelet monoamine oxidase activity (11) and in severity of their SANS symptoms when compared to those of depressed subjects (12), supporting the validity of the concept of secondary negative symptoms in subjects reporting symptoms of depression.…”

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confidence: 94%

Revisiting the factor structure for positive and negative symptoms: evidence from a large heterogeneous group of psychiatric patients

Toomey

Kremen²,

Simpson³

et al. 1997

AJP

116

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H istorically, there have been numerous efforts to delineate meaningful dimensions of symptoms in schizophrenia. These efforts have recently focused on the characterization of positive versus negative symptoms. Positive symptoms represent a behavioral excess generally considered psychotic (e.g., hallucinations, delusions), while negative symptoms represent a deficiency in normal behavior (e.g., poor eye contact, flat affect). The Scale for the Assessment of Negative Symptoms (SANS) and the Scale for the Assessment of Positive Symptoms (SAPS) are commonly used to rate these symptoms (1). The SANS and SAPS together contain 50 items reflecting individual positive and negative symptoms and nine global ratings summarizing symptom areas. Although a number of factor analytic studies have advanced our understanding of the structure of positive and negative symptoms, most of the work in this area has focused on schizophrenic patients. In addition, most studies have examined global ratings, while less is known about the factor structure of individual items.The organization of the original SANS/SAPS reflects the authors' conception at the time of two broad dimensions characterized by positive and negative symptoms (1). It was thought that these two symptom dimensions could potentially differentiate subtypes of schizophrenia (2). However, numerous studies since the development of the scales have yielded a three-factor structure of the SANS/SAPS global ratings in subjects with schizophrenia: a negative symptom factor (SANS) and two positive symptom factors (SAPS hallucinations/delusions and bizarre behavior/formal thought disorder) (3, 4). Liddle (5) termed this last factor the "disorganization syndrome."In addition to this work, there has been ongoing con-

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“…Thibaut et al [47] have measured higher plasma 3-methoxy-4-hydroxyphenylglycol lev els and lower pHVA levels in deficit as compared with nondeficit patients. Finally, Samson et al [48] have reported that deficit patients, in comparison to nondeficit patients, have a lower plasma monoamine oxydase activity.…”

Section: Familial/sporadic Su Btype Smentioning

confidence: 97%

The Deficit Syndrome of Schizophrenia: Towards Heterogeneity

Thibaut

Petit²

1997

Psychopathology

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Since the turn of the century, psychiatrists have been concerned with both the unity and diversity of schizophrenia. From these early descriptions until now, many authors have attempted to delineate clinically meaningful subtypes within this disorder. In this connection, negative/positive subtyping has generated great interest. Carpenter and his team have emphasized the origin of the negative symptoms observed. They have proposed that primary enduring negative symptoms should be distinguished from transient negative symptoms resulting from treatment, depression or social deprivation and should be termed deficit symptoms. The validity of this subtyping is supported by clinical, biochemical or electrophysiological studies showing differences between deficit and nondeficit patients.

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Platelet monoamine oxidase activity and deficit syndrome schizophrenia

Cited by 10 publications

References 42 publications

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Revisiting the factor structure for positive and negative symptoms: evidence from a large heterogeneous group of psychiatric patients

The Deficit Syndrome of Schizophrenia: Towards Heterogeneity

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