tryptamine/атрофия

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Repurposing an orally available drug for the treatment of geographic atrophy.

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OBJECTIVE Chronic oxidative stress and subacute inflammation have been implicated as causes of age-related macular degeneration (AMD). In this study, we tested whether an orally available 5-OH-tryptamine (5HT) 1a receptor agonist, xaliproden, could protect against retinal pigment epithelium (RPE)

Inhibition of the alpha-ketoglutarate dehydrogenase and pyruvate dehydrogenase complexes by a putative aberrant metabolite of serotonin, tryptamine-4,5-dione.

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A transient energy impairment with resultant release and subsequent reuptake of 5-hydroxytryptamine (5-HT) and NMDA receptor activation with consequent cytoplasmic superoxide (O(2)(-)(*)), nitric oxide (NO(*)), and peroxynitrite (ONOO(-)) generation have all been implicated in a neurotoxic cascade

Neurotoxic effects of partially oxidized serotonin: tryptamine-4,5-dione.

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Neurotoxicity of tryptamine-4,5-dione (4,5-DKT), a partially oxidized form of serotonin, was assessed after microinjection into the lateral ventricle, hippocampus, or cingulate cortex of rats followed by Fink-Heimer staining for axon terminal degeneration. Intracerebroventricular injections of

Effect of intranigral administration of 6-hydroxydopamine and 5,7-dihydroxytryptamine on rat brain tryptamine.

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Earlier experiments have shown that unilateral electrolytic lesions of the substantia nigra result in significant reductions in the rate of accumulation of rat striatal tryptamine. For elucidation of the type of neuronal degeneration that is associated with tryptamine depletion, the effects of

Tryptamine depletion in the rat striatum following electrolytic lesions of the substantia nigra.

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Tryptamine is an indolic compound that occurs naturally in the mammalian central nervous system. To test whether tryptamine-containing neurons are present in the nigrostriatal system, we investigated effects of unilateral electrolytic lesions of the substantia nigra on striatal tryptamine

Tryptamine-4,5-dione, a putative endotoxic metabolite of the superoxide-mediated oxidation of serotonin, is a mitochondrial toxin: possible implications in neurodegenerative brain disorders.

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The release and subsequent reuptake of 5-hydroxytryptamine (5-HT) and cytoplasmic superoxide (O2-*) generation have both been implicated as important factors associated with the degeneration of serotonergic neurons evoked by methamphetamine (MA) and cerebral ischemia-reperfusion (I-R). Such

Reactions of the putative neurotoxin tryptamine-4,5-dione with L-cysteine and other thiols.

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Tryptamine-4,5-dione (1) is formed by oxidation of 5-hydroxytryptamine by reactive oxygen and reactive nitrogen species. Dione 1 is a powerful electrophile that can covalently modify cysteinyl residues of proteins and deactivate key enzymes. Thus, 1 has been suggested to play a role in the

Tryptamine induces tryptophanyl-tRNA synthetase-mediated neurodegeneration with neurofibrillary tangles in human cell and mouse models.

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The neuropathological hallmarks of Alzheimer's disease (AD) and other taupathies include neurofibrillary tangles and plaques. Despite the fact that only 2-10% of AD cases are associated with genetic mutations, no nontransgenic or metabolic models have been generated to date. The findings of

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy.

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Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide.

The effect of reduced neopterin on the synthesis of several methylated indoles in the pineal gland of adult male golden hamsters, kept under standardized conditions.

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In the present study the effect was tested of reduced neopterin (RN) on the methylating capacity of the pineal gland of adult, male golden hamsters, housed under standardized conditions throughout the year. An effect of RN on the synthesis of a number of methylated compounds was, indeed,

Synthesis of radiolabelled 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo), a neurotoxic chloral-derived mammalian alkaloid, and its biodistribution in rats.

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Chloral hydrate, the oldest synthetic hypnotic, is still among the most common agents used for conscious sedation of infants and children. Chloral (Clo) spontaneously condenses with the biogenic amine tryptamine (Ta) giving rise to the endogenous formation of

Altered consciousness states and endogenous psychoses: a common molecular pathway?

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Interest in the role of indolamines in the pathogenesis of psychoses has been renewed in recent years by the development of atypical antipsychotic drugs such as clozapine, olanzapine, and risperidone, which act on serotonin receptors. Discovery of the hallucinogenic compounds called methylated

Systemic treatment with a 5HT1a agonist induces anti-oxidant protection and preserves the retina from mitochondrial oxidative stress.

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Chronic oxidative stress contributes to age related diseases including age related macular degeneration (AMD). Earlier work showed that the 5-hydroxy-tryptamine 1a (5HT1a) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) protects retinal pigment epithelium (RPE) cells from

5-hydroxy-3-ethylamino-2-oxindole is not formed in rat brain following a neurotoxic dose of methamphetamine: evidence that methamphetamine does not induce the hydroxyl radical-mediated oxidation of serotonin.

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Oxygen radicals have been implicated in the neurodegenerative and other neurobiological effects evoked by methamphetamine (MA) in the brain. It has been reported that shortly after a single large subcutaneous dose of MA to the rat, the serotonergic neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) is

Neurotoxic indoleamines and monoamine neurons.

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In 1968 Thoenen & Tranzer (1) discovered that the long-lasting depletion of NA in sympathetically innervated organs by 6-OH-DA is due to degeneration of NA terminals. This provided the basis for the development of a new concept in neurobiological research: the method of selective chemical

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