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tryptamine/atrophy

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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)
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
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 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
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
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
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.
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,
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
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
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
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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