Monoaminergic neurotransmitters, their precursors and metabolites in brains of Alzheimer patients

Storga, D.; Vrecko, Karoline; Birkmayer, Joerg George; Reibnegger, Gilbert

doi:10.1016/0304-3940(95)12256-7

Cited by 184 publications

(112 citation statements)

References 18 publications

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“…The literature data on tryptophan concentrations in body fluids and brain of patients with AD are inconsistent. The majority of studies have found low tryptophan concentrations in serum (Widner et al 2000), plasma (Fekkes et al 1998) and CSF (Tohgi et al 1992) while other studies showed no alterations in tryptophan concentrations in plasma (Fonteh et al 2007) and brain (Storga et al 1996) in patients with AD. Low plasma tryptophan concentration might be also a consequence of the enhanced tryptophan degradation via the kynuramine pathway (Widner et al 2000), since a dysregulation of both serotonergic and kynuramine pathways of tryptophan metabolism have been associated with pathophysiology of AD (Ruddick et al 2006).…”

Section: Discussionmentioning

confidence: 97%

Platelet serotonin concentration and monoamine oxidase type B activity in female patients in early, middle and late phase of Alzheimer's disease

Mück‐Šeler

Presečki

Mímica

et al. 2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Section: Discussionmentioning

confidence: 97%

Platelet serotonin concentration and monoamine oxidase type B activity in female patients in early, middle and late phase of Alzheimer's disease

Mück‐Šeler

Presečki

Mímica

et al. 2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Deficiencies in central serotonergic [12][13][14][15] and perhaps dopaminergic [16], but see also [17,18] neural transmission may also play a critical role in some of the clinical manifestations of AD. Significant reductions in γ-amino butyric acid (GABA) levels have also been described in cases of AD [19].…”

Section: Introductionmentioning

confidence: 99%

Altered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease

Aisa

Gil-Bea

Solas

et al. 2010

JAD

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Abstract. Neurotransmitter system dysfunction and synapse loss have been recognized as hallmarks of Alzheimer's disease (AD). Our hypothesis is that specific neurochemical populations of neurons might be more vulnerable to degeneration in AD due to particular deficits in synaptic plasticity. We have studied, in postmortem brain tissue, the relationship between levels of synaptic markers (NCAM and BDNF), neurochemical measurements (cholinacetyltransferase activity, serotonin, dopamine, GABA, and glutamate levels), and clinical data (cognitive status measured as MMSE score). NCAM levels in frontal and temporal cortex from AD patients were significantly lower than control patients. Interestingly, these reductions in NCAM levels were associated to an ApoE4 genotype. Levels of BDNF were also significantly reduced in both frontal and temporal regions in AD patients. The ratio between plasticity markers and neurochemical measurements was used to study which of the neurochemical populations was particularly associated to plasticity changes. In both the frontal and temporal cortex, there was a significant reduction in the ChAT/NCAM ratio in AD samples compared to controls. None of the ratios to BDNF were different between control and AD samples. Furthermore, Pearson's product moment showed a significant positive correlation between MMSE score and the ChAT/NCAM ratio in frontal cortex (n = 19; r = 0.526*; p = 0.037) as well as in temporal cortex (n = 19; r = 0.601*; p = 0.018) in AD patients. Altogether, these data suggest a potential involvement of NCAM expressing neurons in the cognitive deficits in AD.

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“…Although neuritic plaques and their amyloid components continue to play a critical role in the diagnosis of Alzheimer's disease (AD), semi-quantitative studies in groups of normalaged and AD patients have reported that these so-called neuropathological markers of AD also occur to varying degrees in cortical tissue during normal aging, and that their accumulation does not directly correlate with the progression of dementia (Mirra et al 1993;McKeel et al 2004;Tiraboschi et al 2004). Stereological and neurochemical studies of brain tissue from patients with AD have confirmed widespread astrocytosis and microgliosis in cortical brain regions and significant reductions in neurotransmitter-specific subcortical nuclei, including the locus coeruleus (LC) and dorsal raphe (DR), and diminished concentrations in their cortical projections of corresponding monoamine neurotransmitters, norepinephrine (NE) and 5-hydroxytrptamine (5-HT); in contrast, these parameters remain relatively stable in brains of persons that undergo normal (non-demented) brain aging (Aletrino et al 1992;Mouton et al 1994;Storga et al 1996;Zarow et al 2003;Tuppo and Arias 2005). The strongest correlations with dementia severity have been reported in the loss of cortical volume (atrophy), observed by either ante-mortem or post-mortem analyses, and the reduction in cortical synapses (de la Monte 1989;DeKosky and Scheff 1990;Terry et al 1991;Convit et al 1993;Jobst et al 1994;Stout et al 1996;Mouton et al 1998;Zarow et al 2003;de Leon et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Neuropathological quantification of dtg APP/PS1: neuroimaging, stereology, and biochemistry

Manaye

Wang

O’Neil

et al. 2007

AGE

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Murine models that mimic the neuropathology of Alzheimer's disease (AD) have the potential to provide insight into the pathogenesis of the disease and lead to new strategies for the therapeutic management of afflicted patients. We used magnetic resonance imaging (MRI), design-based stereology, and high performance liquid chromatography (HPLC) to assess the age-related neuropathology in double transgenic mice that overexpress two AD-related proteins-amyloid precursor protein (APP) and presenilin 1 (PS1)-and age-and gender-matched wild-type (WT) controls. In mice ranging in age from 4-28 months, total volumes of the hippocampal formation (V HF ) and whole brain (V brain ) were quantified by the Cavalieri-point counting method on a systematic-random sample of coronal T2-weighted MRI images; the same stereological methods were used to quantify V HF and V brain after perfusion and histological processing. To assess changes in ADtype beta-amyloid (Aβ) plaques, sections from the hippocampal formation and amylgdaloid complex of mice aged 5, 12, and 15 months were stained by Congo Red histochemistry. In aged mice with large numbers of amyloid plaques, systematic-random samples of sections were stained by GFAP immunocytochemistry to assess gender and genotype effects on total numbers of astrocytes. In addition, levels of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and 5-HT metabolites were assayed by HPLC in fresh-frozen samples from neocortex, striatum, hippocampus, and brainstem. We confirmed age-related increases in amyloid plaques, beginning with a few plaques at 5 months of age and increasing densities by AGE (2007) 12 and 15 months. At 15 months of age, there were robust genotype effects, but no gender effects, on GFAP-immunopositive astrocytes in the amygdaloid complex and hippocampus. There were no effects on monoamine levels in all brain regions examined, and no volume changes in hippocampal formation or whole brain as quantified on either neuroimages or tissue sections. Strong correlations were present between volume estimates from MRI images and histological sections, with about 85% reduction in mean V HF or mean V brain between MRI and processed histological sections. In summary, these findings show that the double transgenic expression of AD-type mutations is associated with age-related increases in amyloid plaques and astrocytosis; however, this model does not recapitulate the cortical atrophy or neurochemical changes that are characteristic of AD.29:87-96 DOI 10.1007/s11357-007-9035-

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Monoaminergic neurotransmitters, their precursors and metabolites in brains of Alzheimer patients

Cited by 184 publications

References 18 publications

Platelet serotonin concentration and monoamine oxidase type B activity in female patients in early, middle and late phase of Alzheimer's disease

Platelet serotonin concentration and monoamine oxidase type B activity in female patients in early, middle and late phase of Alzheimer's disease

Altered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease

Neuropathological quantification of dtg APP/PS1: neuroimaging, stereology, and biochemistry

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