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serotonin/atrofi

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Plasma serotonin is a predictor for deterioration of urinary albumin excretion in men with type 2 diabetes mellitus.

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We performed an observational study to investigate if plasma 5-hydroxyindole-3-acetic acid (5-HIAA), a derivative end product of serotonin (5-hydroxytryptamine), concentration could be a predictor for deterioration of urinary albumin excretion. The relationship between baseline plasma 5-HIAA

Serotonin transporter availability in early stage Parkinson's disease and multiple system atrophy.

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Background. Differentiating Parkinson's disease (PD) from multiple system atrophy (MSA) can be challenging especially early in the course of the disease. Previous studies have shown that midbrain serotonin transporter (SERT) availability in patients with established MSA was significantly lower

Degeneration of serotonin-specific neurons in the brain in experimental Trypanosoma brucei infection.

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ORMEROD and HUSSEIN (1986) have shown that an intracellular stage of Trypanosoma brucei rhodesiense causes the destruction of ependymal cells lining the ventricles of the brain. The ventricular ependymal cells are intimately associated with a plexus of nerves that react specifically with monoclonal

Systemic glutamate induces degeneration of a subpopulation of serotonin-immunoreactive neurons in the area postrema of rats.

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Neuronal damage in the area postrema (AP) of adult Sprague-Dawley rats was induced by subcutaneous administration of monosodium glutamate (MSG; 9 mg/g b.wt.). Serotonin-immunoreactive (5-HT-IR) neurons were visualized in the AP 3 h or 7 days after control or MSG treatment. At 3 h post MSG, many

Spinal cord interneuron degenerative atrophy caused by peripheral nerve lesions is prevented by serotonin depletion.

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Peripheral nerve section causes a degenerative atrophy of substance P sensory input and of met-enkephalin interneurons in the dorsal horn of the spinal cord. Radioimmunoassay of both peptides indicates that the decrease in peptide levels ranges from 30 to 50%, that it occurs several days after

The neurotoxin 2'-NH2-MPTP degenerates serotonin axons and evokes increases in hippocampal BDNF.

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1-Methyl-4-(2'-aminophenyl)-1,2,3,6-tetrahydropyridine (2'-NH2-MPTP) causes long-term depletions in cortical and hippocampal serotonin (5-HT) and norepinephrine (NE) that are accompanied by acute elevations in glial fibrillary acidic protein (GFAP) and argyrophilia. To further investigate the

Reduced vesicular monoamine transport disrupts serotonin signaling but does not cause serotonergic degeneration.

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We previously demonstrated that mice with reduced expression of the vesicular monoamine transporter 2 (VMAT2 LO) undergo age-related degeneration of the catecholamine-producing neurons of the substantia nigra pars compacta and locus ceruleus and exhibit motor disturbances and depressive-like
Beas-Zarate and coworkers (Eur. J. Pharmacol., 198 (1991) 7-14) recently reported markedly reduced concentration of presynaptic serotonin neurotransmitter markers in cerebellum of rodents which had suffered destruction of the inferior olivary-cerebellar (climbing fibre) projections by the neurotoxin
Reactive oxygen species play an important role in the pathogenesis of diabetic retinopathy. We studied the role of adrenergic and serotonin receptors in the generation of superoxide by retina and 661W retinal cells in high glucose and of the α1-adrenergic receptor (AR) on vascular lesions of the
Late-life depression, even when of subsyndromal severity, has shown strong associations with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Preclinical studies have suggested that serotonin selective reuptake inhibitors (SSRIs) can attenuate amyloidogenesis. Therefore, we aimed to
Microglia are the resident mononuclear phagocytes of the central nervous system and have been implicated in the pathogenesis of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). During neurodegeneration, microglial activation is accompanied by infiltration of circulating

Effect of GM1 ganglioside on neonatally neurotoxin induced degeneration of serotonin neurons in the rat brain.

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The effect of exogenous GM1 ganglioside on the 5,7-dihydroxytryptamine (5,7-HT; a selective serotonin neurotoxin) induced alteration of the postnatal development of central 5-hydroxytryptamine (5-HT; serotonin) neurons has been investigated using neuro-chemical and immunocytochemical techniques.

Blocking of striated muscle degeneration by serotonin in C. elegans.

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Prevention of muscle fiber degeneration is a key issue in the treatment of muscular dystrophies such as Duchenne Muscular Dystrophy (DMD). It is widely postulated that existing pharmaceutical compounds might potentially be beneficial to DMD patients, but tools to identify them are lacking. Here, by

Experimental serotonin myopathy as an animal model of muscle degeneration and regeneration in muscular dystrophy.

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Degenerating and regenerating muscle fibers, in serotonin-induced myopathy (SM) of rats, were investigated histochemically, immunohistochemically and electron microscopically with polyclonal antibodies against dystrophin, type IV collagen and laminin. The myopathy produced was characterized by
Frontotemporal lobar degeneration (FTLD) is a progressive neurodegenerative disorder characterized by behavioral and language disturbances. We performed a case-control association study in the Italian population to assess the relevance for FTLD genetic susceptibility of the serotonin (5-HT)
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