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Neurochemical Mechanisms in Disease P20

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site just above the extracellular gate (Singh et al., 2007. Zhou et al., 2007). Vesicular uptake is coupled to a proton gradient across the vesicle membrane rather than the sodium gradient used with the plasma membrane transporters (Schuldiner et al., 1995). Henry et al., 1998).. VMAT is predicted to have similar membrane topology to the plasma mem- brane monoamine transporters,...

Neurochemical Mechanisms in Disease P21

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Parkinson’s disease (PD) is characterized by rigidity in movement, resting tremor, bradykinesia, and difficulty in maintaining postural stability (Gelb et al., 1999). PD is a neurodegenerative disease marked by Lewy bodies or abnormal protein aggre- gates and the loss of dopaminergic cells in the substantia nigra (Gelb et al., 1999).. However, the progressive loss of dopaminergic neurons has led researchers...

Neurochemical Mechanisms in Disease P22

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Abstract Diseases of the brain account for much human suffering and place a huge burden on the health care systems. As evident from this chapter, failure of the metabolic homeostasis of the two amino acids of major importance, namely glutamate and glu- tamine, is a hallmark of a wide range of both neurological and psychiatric diseases.. Bak et al.. 2...

Neurochemical Mechanisms in Disease P23

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of dopaminergic pathways and cause Parkinsonism) treatment of cats and NMRS analysis found lower [glutamate+glutamine]/[creatine] ratio than in control animals (Podell et al., 2003).. inhibits succinate dehydrogenase, a TCA cycle enzyme) induces lesions in the stria- tum of animals leading to symptoms similar to Huntington’s disease in humans (Brouillet et al., 1998). However, this selective inhibition of (GABAergic) neuronal function...

Neurochemical Mechanisms in Disease P24

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Poirier et al., 2006). Fiala et al., 2002. Newey et al., 2005. Similar alterations with the presence of long tortuous spines have been observed in other defined classes of MR, such as fragile-X syndrome (Rudelli et al., 1985. Hinton et al., 1991. Wisniewski et al., 1991. Irwin et al., 2001). Takashima et al., 1981. Takashima et al., 1994). Subsequent studies...

Neurochemical Mechanisms in Disease P25

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Noteworthy is a recent study that reported PAK3 binds significantly more Cdc42 than Rac1, and is selectively activated by endoge- nous Cdc42, suggesting that PAK3 is a selective effector of Cdc42 (Kreis et al., 2007). Among the PAK proteins, PAK1 and PAK3 are highly expressed in the brain.. Both proteins are present in the hippocampus and cortex, with PAK3 being...

Neurochemical Mechanisms in Disease P26

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Ferrer I, Gullotta F (1990) Down’s syndrome and Alzheimer’s disease: dendritic spine counts in the hippocampus. Fiala JC, Spacek J, Harris KM (2002) Dendritic spine pathology: cause or consequence of neurological disorders? Brain Res Brain Res Rev 39:29–54. Fukazawa Y, Saitoh Y, Ozawa F, Ohta Y, Mizuno K, Inokuchi K (2003) Hippocampal LTP is accompanied by enhanced F-actin content within...

Neurochemical Mechanisms in Disease P27

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Alzheimer’s disease alone is now the third most expensive disease to treat in the United States, costing close to $100 billion annually.. For instance, recent studies have identified that synaptic transmission is one of the earliest events in the cognitive abnormalities that characterize AD and PD. The integration of this information with data-based circuits modeling, in which neuronal electrical properties,...

Neurochemical Mechanisms in Disease P28

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Power is higher in the absence of visual input. Conceive of a person sleeping in the dark, awakened and quickly looking for an invisible visual target. Our inten- tion to see even in the absence of visual stimulus, is a prerequisite for the saccades to start. Perisaccadic phasic gamma in the absence of visual stimulation may rep- resent intrasaccadic cerebral...

Neurochemical Mechanisms in Disease P29

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7 Nondopaminergic Signals and Cognition in PD 7.1 GABA and the Subthalamic Nucleus. However, adverse mood and cognitive effects have been also described and preoperative selection criteria have to be adhered to min- imize the chances for adverse effects (Lang et al., 2006). Some of the results also raised questions concerning our neuroanatomical and neuropharmacological con- cepts of the classical...

Neurochemical Mechanisms in Disease P30

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In a clin- ical setting, functional imaging is basically limited to positron emission tomography (PET), where two modalities are currently used: [18F]fluorodeoxy glucose (FDG) to evaluate brain glucose metabolism (Gonzalez et al., 1995) and more recently imag- ing of amyloid-beta, using Aβ selective carbon-11 labeled thioflavin-T ([C-11]PIB) or stilbene ([C-11]SB-11) compounds. So far in the United States there are only...

Neurochemical Mechanisms in Disease P31

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Di Carlo A, Lamassa M, Baldereschi M, Inzitari M, Scafato E, Farchi G, Inzitari D (2007) CIND and MCI in the Italian elderly: frequency, vascular risk factors, progression to dementia.. Dixon RM, Bradley KM, Budge MM, Styles P, Smith AD (2002) Longitudinal quantitative proton magnetic resonance spectroscopy of the hippocampus in Alzheimer’s disease. Dujardin K, Defebvre L, Grunberg C (2001)...

Neurochemical Mechanisms in Disease P32

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2 Structure of NF- κ B and I κ B Family. The homod- imers of p50 and p52, and the p50/p52 heterodimer may occupy the NF-κB–binding sites of DNA and, thus, function as repressors of gene transcription (Franzoso et al., 1992). NF-κB exists in the cytoplasm in an inactive form via association with the inhibitor of NF-κB (IκB) proteins. The...

Neurochemical Mechanisms in Disease P33

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6 Role of NF- κ B in Brain Diseases. The diseases in which abnormal NF-κB regulation has been reported to play significant roles include atherosclerosis, AIDS, tumors, diabetes, heart dis- eases, muscular dystrophy, rheumatoid arthritis, inflammatory bowel diseases, bone resorption, and some neurodegenerative diseases reviewed by (Kumar et al., 2004).. 6.1 Role of NF- κ B in Ischemic and Traumatic...

Neurochemical Mechanisms in Disease P34

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NF-κB in Brain Diseases 315 Monaco C, Paleolog E (2004) Nuclear factor kappaB: a potential therapeutic target in atheroscle-. Mukhopadhyay A, Manna SK, Aggarwal BB (2000) Pervanadate-induced nuclear factor-kappaB activation requires tyrosine phosphorylation and degradation of IkappaBalpha. Nakajima K, Kikuchi Y, Ikoma E, Honda S, Ishikawa M et al (1998) Neurotrophins regulate the function of cultured microglia. Oncogene Nonaka M,...

Neurochemical Mechanisms in Disease P35

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et al., 1998). Myotonia and progressive muscle weakness are characteristics of the adult-onset disease. Developmental and mental abnormalities together with hypotonia and respiratory distress are characteristics of the more severe congenital disease. DM1 transcripts have been shown to accumulate in the nuclei of muscle cells (Jiang et al., 2004). In DM1, proteins in the muscleblind family are recruited to these...

Neurochemical Mechanisms in Disease P36

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proteinaceous deposits are especially prominent in this disease (Rolfs et al., 2003).. The disease is interesting because some patients present first with exclusively pure psychiatric symptoms while having no signs of ataxia or movement disorders (Rolfs et al., 2003). The authors point out that SCA17 represents one of the very few psychiatric diseases for which there is a known monogenic...

Neurochemical Mechanisms in Disease P37

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Table 3 A n -expansion diseases. Transcription factor . Two A n - expansion diseases are X-linked. A mutation in the SOX3 gene, giving rise to sex-linked mental retardation (MRX) with growth hormone deficiency, has been described in one large family (Brown and Brown, 2004). A n -Expansion mutations can occur in two different tracts in the expressed protein of...

Neurochemical Mechanisms in Disease P38

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Quintanilla RA, Johnson GVW (2009) Role of mitochondrial dysfunction in the pathogenesis of Huntington’s disease. Reddy PH, Mao P, Manczak M (2009) Mitochondrial structural and functional dynamics in Huntington’s disease. N, Raskin S, Werneck LC, Junior WM, Tumas V (2008) Huntington’s disease-like 2 in Brazil – report of 4 patients. Rose C, Menzies FM, Renna M, Acevedo-Arozena A, Corrochano S,...

Neurochemical Mechanisms in Disease P39

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With murine autoimmune encephalomyelitis, overproduction of TGFβ1 locally in the brain led to a more severe and earlier onset of the disease with increased infiltration of mononuclear cells in the brain (Luo et al., 2007). The encephalomyelitis model seems to indicate that the brain will signal to the immune system in certain circumstances as was suggested by increased plasma levels...