China
Africa
Explore chapters and articles related to this topic
Markers of Cholinergic Dysfunction in Alzheimer Disease
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Ezio Giacobini, Kiminobu Sugaya, Rodger J. Elble
Davis et al. (1986) found that AD patients with a senile onset of dementia had a significantly higher concentration of cortisol in plasma than those with presenile onset. CSF nocturnal cortisol and MHPG (3-methoxy-4-hydroxyphenylglycol) concentrations were negatively correlated. Cortisol concentrations at 9 AM were significantly higher in AD patients than in normal subjects. The 9 AM cortisol concentration correlated with severity of dementia but not with age. In order to investigate changes in plasma cortisol levels produced by central cholinergic stimulation due to increased levels of ACh in brain, Kumar et al. (1988) studied the differential effect of two ChE inhibitors, Phy and neostigmine, in a double-blind crossover investigation of AD. Physostigmine (60 μg/kg) increased plasma, cortisol relative to neostigmine (7.5 mg) (a peripherally acting inhibitor that does not penetrate the CNS) with the greatest difference more than 90 min after oral administration. Physostigmine also significantly decreased plasma BuChE activity in the same patients. There was a significant positive correlation between the increase in cortisol and the decrease in ChE activity due to physostigmine but not to neostigmine (Table VI).
Shy-Drager Syndrome and Multiple System Atrophy
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Monoaminergic systems have been evaluated by measuring their respective metabolite levels in CSF. The major brain metabolite of NA is 3-methoxy-4-hydroxyphenylglycol (MHPG). In order to use CSF MHPG levels as an index of central noradrenergic activity, it is necessary to correct the CSF level for the plasma contribution, because free MHPG readily crosses the blood-brain barrier (Kopin et al., 1983a). Patients with MSA have low total CSF MHPG, but normal plasma levels of the metabolite (Polinsky, Jimerson and Kopin, 1984). Thus, the component of CSF MHPG due to central NA metabolism is reduced in MSA, consistent with central nervous system noradrenergic dysfunction. This contrasts with the findings in PAF where the diminished total CSF MHPG level results from a decreased plasma contribution, a reflection of peripheral sympathetic neuronal involvement.
Lithium: Predicting Response/Maximizing Efficacy
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
R. Bruce Lydiard, Rowland Pearsall
The catecholamine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) has been widely studied as an index of CNS norepinephrine (NE) activity. The MHPG metabolite derives both from CNS and peripheral metabolism of NE and the ratio of contribution to urinary MHPG excretion is unclear.113,114 However, even if the majority of MHPG is derived from peripheral sources, determination of urinary MHPG could still empirically be a useful clinical tool.114,115 MHPG excretion in the urine is most reliably measured by collecting a 24-hr urine sample after the patient has been on a low monoamine diet. Studies over the past few years have also attempted to measure plasma MHPG concentrations. Both plasma and urine MHPG levels appear to change and correlate with mood changes in affective states.116
Association study of Catechol-O-Methyltransferase (COMT) rs4680 Val158Met gene polymorphism and suicide attempt in Mexican adolescents with major depressive disorder
Published in Nordic Journal of Psychiatry, 2022
Marco Antonio Sanabrais-Jiménez, Alejandro Aguilar-García, Sandra Hernández-Muñoz, Emmanuel Sarmiento, Rosa E. Ulloa, Anabel Jiménez-Anguiano, Beatriz Camarena
The serotonergic system was first implicated in the etiology of suicidal behavior, which supported the findings of low 5-hydroxyindoleacetic acid in the cerebrospinal fluid in suicide subjects [7]. An independent association has been reported with a low serotonergic activity between suicidal behavior and major depressive disorder [8]. It was reported differences in binding values of several serotonin receptor subtypes and serotonin transporter in the brain of suicide victims compared with non-suicidal victims [9]. Furthermore, the catecholaminergic system has been linked to suicidal behavior based on reports showing low homovanillic acid levels in cerebrospinal fluid of depressed patients with a history of SA [10,11]. Also, low levels of 3-methoxy-4-hydroxyphenylglycol, a metabolite of norepinephrine, were detected in SA subjects [12]. The neurobiological findings suggest that genes related to serotonergic and catecholaminergic systems are involved in the development of SA.
Identifying and responding to fatigue and apathy in Parkinson’s disease: a review of current practice
Published in Expert Review of Neurotherapeutics, 2020
Claudia Lazcano-Ocampo, Yi Min Wan, Daniel J van Wamelen, Lucia Batzu, Iro Boura, Nataliya Titova, Valentina Leta, Mubasher Qamar, Pablo Martinez-Martin, K Ray Chaudhuri
On the other hand, the relationship between apathy and executive function [22], depression [21,22], and sleep disturbances [22] implicates additional non-dopaminergic origins. Mayeux et al. found a correlation between the CSF concentration of 3-methoxy-4-hydroxyphenylglycol (MHPG), the major metabolite of noradrenaline, and cognitive measures of bradyphrenia [49], which advocates that bradyphrenia (which is similar to the concept of apathy) in PD may be related to dysfunction of catecholaminergic pathways and the locus coeruleus. Evidence of a disruption in the serotonergic systems is also revealed by the 2016 study in de novo PD, when 15 patients with apathy primarily demonstrated greater serotonergic alteration in the ventral striatum, the dorsal, and the subgenual parts of the bilateral anterior cingulate cortices, as well as in the right-sided caudate nucleus and the right-sided orbitofrontal cortex, as compared to those without apathy [50]. Finally, the cholinergic systems may also play a vital modifying role on motivation in PD, given the robust link between PD apathy and cognitive impairment which is elaborated later in this text, and also based on the therapeutic benefit of cholinesterase inhibitors for treating apathetic behavior in some without depression and dementia [51].
Mirtazapine for chronic breathlessness? A review of mechanistic insights and therapeutic potential
Published in Expert Review of Respiratory Medicine, 2019
N. Lovell, A Wilcock, S Bajwah, S. N. Etkind, C. J. Jolley, M Maddocks, I. J. Higginson
NE is important in neuronal connections between the amygdala and the locus coeruleus, the center involved in generating the physiological response to stress and panic, e.g. increased heart rate, blood pressure and respiratory rate [57]. While the role of NE during an acute stress is hyperactivity, chronic stress (for example, in mood disorders) causes hypo-reactivity of the NE system [77], and in animal studies exposure to chronic stress has been correlated with a decrease in the release of NE in the brain, as well as atrophy of NE axonal projections [78,79]. Further, venoarterial levels of NE and 3-methoxy-4-hydroxyphenylglycol (the metabolite of NE) are significantly lower in people diagnosed with depression compared to controls [80]. In addition, a rise in circulating norepinephrine causes relaxation of bronchial muscles and a decrease in fluid secretion from bronchial glands, therefore, improving respiration [81,82]. Other neurotransmitters of interest include endorphins [83], cannabinoids, and neurokinin [84].