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Brain postmortem studies

Goodwin LR, Francom D, Dieken FP, et al. 1989. Determination of sulfide in brain tissue by gas dialysis/ion chromatography Postmortem studies and two case reports. J Anal Toxicol 13 105-109. [Pg.185]

Proteins involved in the fundamental structure and function of neurons are decreased in schizophrenia. Several postmortem studies have identified consistent reductions in the expression of mitochondrial associated genes involved in oxidative metabolism, such as cytochrome oxidase and cytochrome C reductase [23], Reduced oxidative metabolism is consistent with evidence of increased brain lactate,... [Pg.883]

Serotonergic function has been investigated by using multiple methods. Assaying the major metabolite of serotonin, 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF) has been widely used (Ch. 13). This method assumes that CSF 5-HIAA is related to brain serotonin activity. This premise is supported by the rostral-caudal concentration gradient of CSF 5-HIAA and the observation in postmortem studies that CSF 5-HIAA correlates with levels of 5-HIAA in prefrontal cortex [16], both of which suggest that CSF 5-HIAA is a reasonable index of prefrontal serotonin turnover. ... [Pg.889]

Other abnormalities are more trait-like, and persist following symptom remission. They are found in orbital and medial prefrontal cortex areas where postmortem studies have also documented reductions in cortex volume and histopathologic changes in primary mood disorders [68], Evidence from brain mapping, lesion analysis and electrophysiologic studies of humans and experimental... [Pg.894]

The etiologies of the neurodegenerative diseases are still largely unknown but, especially for AD and PD, postmortem studies have shown clear links between the disease and a deficiency of neurotransmitters in some parts of the brain. Thus, in PD there is a chronic shortage of dopamine... [Pg.378]

J.O. Rinne, T. Myllykyla, P. Ldnnberg, P. MarjamakI, A postmortem study of brain nicotinic receptors In Parkinson s and Alzheimer s disease. Brain Res. 547 (1991) 167-170. [Pg.82]

Advances in this area have perhaps been the most profound over the past 5 to 10 years, occurring as a result of imaging studies followed by focused postmortem studies of the brains of patients with both bipolar and unipolar depression. Neuroimaging studies of patients with familial pure major depression have identified neurophysiological abnormalities in multiple areas of the orbital and medial prefrontal cortex (PFC), the amygdala, and related parts of the striatum and thalamus. Some of these abnormalities appear to be state dependent (i.e., present only when the patient is clinically depressed), whereas other abnormalities appear to be trait dependent (i.e., present whether the patient is depressed or not) ( 27). [Pg.114]

Nazarali AJ, Reynolds GP (1992) Monoamine neurotransmitters and their metabolites in brain regions in Alzheimer s disease a postmortem study. Cell. Mol. Neurobiol. 12 581-587. [Pg.40]

Indeed, there is a correlation between impaired NE transmission and depressive behavior. Postmortem studies demonstrated increased NE levels in the brains of unipolar and bipolar suicide victims (Juckel et al., 2000 Wiste et al., 2008). One positron emission tomography (PET) study suggested that depressive patients have an increased activity of MAO-A, which might result in reduced catecholamine levels (Meyer et al., 2006). Another imaging study showed correlation between the degree of loss of limbic NE innervation and severity of depressive symptoms in Parkinson patients (Brooks and Piccini 2006 Remy et al., 2005). [Pg.373]

Finally, other factors but the onconeural antibodies may predispose an individual to neuronal damage or contribute to inflammation. We have reported lack of expression of the complement regulator protein CD59 on the surface of Purkinje cells in individuals with PCD, indicating vulnerability to the effects of complement activation [202]. Complement depositis have been found in the brain stem of a patient with paraneoplastic OM [80], Others have found absent or weak complement deposition in postmortem studies of the brain of PEM/SN patients [41, 203, 204], suggesting that... [Pg.167]

Striatum Many postmortem studies have focused on DA receptor expression in the striatum, due to its high expression of D and D2 receptors, the importance of D2 receptors in the treatment of schizophrenia, and the involvement of the striatum in generating extrapyramidal side effects. Several studies of striatal expression of both Dr and D2-type receptors in postmortem brain did not find altered expression of transcripts for any of these receptors in schizophrenia ( Table 4.2-1) (Roberts et al., 1994, 1996 Harrington et al., 1995 Meador-Woodruff et al., 1997 Stefanis et al., 1998). In addition, one study measured D2 protein expression, reporting unaltered levels of this receptor in the caudate and putamen (Dean et al., 2004). [Pg.446]

Abi-Dargham A, Laruelle M, Lipska B, Jaskiw GE, Wong DT, Robertson DW, Weinberger DR, Kleinman JE. 1993. Serotonin 5-HT3 receptors in schizophrenia A postmortem study of the amygdala. Brain Res 616(1-2) 53-57. [Pg.475]

Little KY, McLaughlin DP, Zhang L, McFinton PR, Dalack GW, Cook EH, Jr, Cassin BJ, Watson SJ (1998b) Brain dopamine transporter messenger RNA and binding sites in cocaine users a postmortem study. Arch Gen... [Pg.566]

Ramakrishnan P, Dickson DW, Davies P (2003) Pinl colocahzation with phosphorylated tau in Alzheimer s disease and other tauopathies. Neurobiol Dis 14 251-264 Rapoport SI (1999) In vivo PET imaging and postmortem studies suggest potentially reversible and irreversible stages of brain metabohc failure in Alzheimer s disease. Eur Arch Psychiatry CUn Neurosci 249(Suppl 3) 46-55... [Pg.603]


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