Cerebrospinal monoamine metabolites and amino acid content in patients with parkinsonian syndrome and rats lesioned with MPP+

Abstract

Monoamine metabolites and amino acid concentration in cerebrospinal fluid (CSF) of 33 untreated patients with parkinsonian syndrome, and 20 control patients without specific neurological symptoms have been compared with those obtained in cerebrospinal fluid of rats intrastriatally lesioned with 1-methyl-4-phenylpyridinium ion (MPP+) and sham operated animals. Homovanillic acid content was found to be significantly lower in patients with severe parkinsonism (motor score of UPDRS > 24), but not in patients with mild symptoms (motor score < or = 24). A correlation between the loss of striatal dopamine and the decrease in cerebrospinal homovanillic acid has been established in rats treated with MPP+. The extrapolation of these results to those obtained from human patients could be important in assessing the degree of striatal dopamine loss shown by humans with parkinsonian syndrome at the moment of clinical diagnosis. No significant differences were found between the other monoamine metabolites analyzed and free amino acid content in human and rat CSF.

Striatal Alterations of Secretogranin-1, Somatostatin, Prodynorphin, and Cholecystokinin Peptides in an Experimental Mouse Model of Parkinson Disease

“…Studies on animal models of PD showed an increase of somatostatin mRNA in unilaterally lesioned primates and rats (56,57). Our present results are in line with the significant increase of somatostatin-like immunoreactivity levels investigated in cerebrospinal fluid (CSF) from 23 patients with untreated early parkinsonian syndrome compared with control subjects (58). However, the opposite was found in CSF of patients with moderate or severe disease (59).…”

CSF somatostatin increase in patients with early parkinsonian syndrome

“…HVA is one of the main metabolites of dopamine in the CNS, and it may thus reflect the dopaminergic central function. There is general agreement in the literature about a decrease in the levels of CSF-HVA in patients with IPD (LeWitt et al, 1992), with a strong negative correlation with the motor disability and the duration of the disease (Tohgi et al, 1993;Chia et al, 1993;Espino et al, 1994). However, although CSF-HVA levels were lower in our patients than in controls, the difference was not significant.…”

Cerebrospinal fluid biochemical studies in patients with Parkinson's disease: toward a potential search for biomarkers for this disease

“…Normality of CSF glutamate levels has been reported by most investigators (Van Sande et al, 1971; Gjessing et al, 1974; Lakke and Teelken, 1976; Lakke et al, 1987; Perschak et al, 1987; Espino et al, 1994; Jiménez-Jiménez et al, 1996; Kuiper et al, 2000), although 3 groups described decreased CSF glutamate levels (Gründig and Gerstenbrand, 1980; Tohgi et al, 1991c; Mally et al, 1997), while CSF glutamine (the main precursor of glutamate) has been found to be normal (Gjessing et al, 1974; Lakke and Teelken, 1976; Manyam et al, 1988; Jiménez-Jiménez et al, 1996) or increased (Mally et al, 1997). …”

“…Engelborghs et al (2003) reported normal CSF DA and HVA, and decreased DOPAC levels. González-Quevedo et al (1993) described normal CSF HVA levels, Espino et al (1994) found decreased HVA only in advanced but not in early PD, Parkinson Study Group DATATOP Investigators found normal levels in early PD (LeWitt et al, 2011). Zubenko et al (1986) described a non-significant trend toward decreased CSF HVA levels in demented PD patients compared with controls.…”