Disease relevance of Romotal

• The symptoms and signs of the condition were reversed by the intravenous administration of the cholinesterase-inhibitor tetrahydroaminacrine [1].
• Moreover, tetrahydroaminoacridine markedly produced cholinomimetic side-effects, such as hypothermia, tremor, miosis and lacrimation [2].
• Effect of tetrahydroaminoacridine, a cholinesterase inhibitor, on cognitive performance following experimental brain injury [3].
• Although both compounds had anti-amnesic effect against scopolamine-induced memory impairment, THA also induced catalepsy in rats [4].
• Genetic toxicity studies of 1,2,3,4-tetrahydro-9-acridinamine (tacrine) [5].

Psychiatry related information on Romotal

• We treated 17 patients who had moderate to severe Alzheimer's disease with oral tetrahydroaminoacridine (THA), a centrally active anticholinesterase, in a three-phase study [6].
• This paper examines inhibition of acetylcholinesterase (AchE) and butyrylcholinesterase (BuchE) by tetrahydroaminoacridine (THA), an acridine analog under consideration for palliative treatment of Alzheimer's dementia [7].
• Cholinesterase inhibitors, such as physostigmine and tetrahydroaminoacridine, have been found to alleviate some of the memory deficits characteristic of senile dementia of the Alzheimer's type (SDAT) [8].
• Tetrahydroaminoacridine antagonism to narcotic addiction [9].
• Tetrahydroaminoacridine facilitates passive avoidance learning in rats with nucleus basalis magnocellularis lesions [10].

High impact information on Romotal

• The efficacy and safety of tacrine (tetrahydroaminoacridine) plus lecithin were studied in a randomised, double-blind, placebo-controlled, crossover study [11].
• Using suspensions of freshly isolated rat hepatocytes, we investigated the mechanism of tetrahydroaminoacridine cytotoxicity by examining the effect of tetrahydroaminoacridine on hepatocyte viability, protein synthesis, protein, DNA and RNA levels and ultrastructure [12].
• We found that viable, tetrahydroaminoacridine-treated hepatocytes (1.0 to 2.0 mmol/L or 118 to 235 micrograms/10(6) cells) demonstrated a dose-dependent and dramatic aggregation of ribosomes on endoplasmic reticulum as well as the aggregation of other nucleic acids found in the nucleus (chromatin) and in mitochondria [12].
• The effect of tetrahydroaminoacridine (THA) on P300 in Alzheimer's disease [13].
• By means of the Hansch approach, QSAR equations were obtained, quantitatively accounting for both the detrimental steric effect of substituents in position 7 and the favorable electron-attracting effect exerted by substituents in positions 6 and 7 of the 9-amino-1,2,3,4-tetrahydroacridine derivatives [14].

Chemical compound and disease context of Romotal

• Tacrine (tetrahydroaminoacridine) is currently the only drug approved for the treatment of Alzheimer's disease [12].
• Double-blind, placebo-controlled investigations of scopolamine, physostigmine, arecoline, and tetrahydroaminoacridine (THA) in normal adults and in dementia of the Alzheimer-type (DAT) were reviewed to determine the relative sensitivity of various assessment procedures in the measurement of drug effects [15].
• The stereotyped behavior induced by apomorphine in rats was inhibited by oxotremorine and tetrahydroaminoacridine (THA) [16].
• The present study examined the efficacy of single and combined treatments with an anticholinesterase, tetrahydroaminoacridine, nicotine and a glycine-B site partial agonist, D-cycloserine, in alleviating the water maze reversal learning defect induced by a medial septal lesion [17].
• Tetrahydroaminoacridine (1 and 3 mg/kg) and nicotine (0.1 and 0.3 mg/kg) had no effect on reversal learning [17].

Biological context of Romotal

• Our preliminary study has shown that age-induced apoptosis of cerebellar granule cells is protected by pretreatment with tetrahydroaminoacridine (THA), an antidementia drug [18].
• Pharmacokinetics of tetrahydroaminoacridine: relations to clinical and biochemical effects in Alzheimer patients [19].
• The data show that tetrahydroaminoacridine increases blood pressure in normotensive freely moving rats by activating central muscarinic cholinergic transmission [20].
• Mechanisms of the tetrahydroaminoacridine effect on action potential and ion currents in myelinated axons [21].
• The tetrahydroaminoacridine-induced reduction in heart rate appears to be due to the increase in vagal tone and plasma vasopressin [20].

Anatomical context of Romotal

• Tetrahydroaminoacridine-induced ribosomal changes and inhibition of protein synthesis in rat hepatocyte suspensions [12].
• The histochemical distribution of cholinesterases in the cerebral cortex and their response to cholinesterase inhibitors such as physostigmine and tetrahydroaminoacridine (THA) were investigated in brains from patients with Alzheimer's disease and control subjects [22].
• Inhibitory effect of 9-amino-1,2,3,4-tetrahydroacridine (THA) on the potassium current of rabbit sinoatrial node [23].
• We administered tetrahydroaminoacridine (THA), a cholinesterase inhibitor, to rats with bilateral nucleus basalis magnocellularis lesions and measured their performance in a spatial learning task [24].
• Comparison of 4-aminopyridine and tetrahydroaminoacridine on basal forebrain neurons [25].

Associations of Romotal with other chemical compounds

• The effects of tetrahydroaminoacridine (THA), 3,4 diaminopyridine (3,4 DAP) and physostigmine were evaluated for their ability to reduce memory impairments in aged, test-sophisticated cebus monkeys (18 to 26 years old) [26].
• Histamine-N-methyltransferase (HNMT), the major enzyme for the metabolism of histamine in rat brain, is potently inhibited by 9-amino-1,2,3,4-tetrahydroacridine (tacrine) [27].
• The effect of bilateral ibotenic acid lesions of the nucleus basalis magnocellularis (NBM) on performance in a step-through passive avoidance task and the ability of tetrahydroaminoacridine (THA) to enhance learning were evaluated [10].
• We investigated the effect of tetrahydroaminoacridine, a cholinesterase inhibitor and D-cycloserine (a partial glycine-B agonist of the NMDA receptor complex) on the defect of water maze spatial navigation in rats induced by aging [28].
• Acute effects of tetrahydroaminoacridine on beta-adrenoceptor-linked cyclic AMP accumulation in brain of young and middle-aged rats [29].

Gene context of Romotal

• Finally, these studies indicate that simultaneous binding of alkylene-linked 9-amino-1,2,3,4-tetrahydroacridine dimers to the catalytic and peripheral sites of AChE is possible with a tether length as short as 5 methylenes [30].
• In vitro protection of acetylcholinesterase and butyrylcholinesterase by tetrahydroaminoacridine. Comparison with physostigmine [31].
• These studies suggest that the inhibitory effect of galanin on cholinergically mediated hypothermia induced by RS86 and tetrahydroaminoacridine may be exerted via an action at ATP-sensitive K+ channels but is unlikely to be acting directly at the site labelled by [3H]glibenclamide [32].
• The effects of oral administration of the PPE were examined with comparison of those of selective butyrylcholinesterase inhibitors of 9-amino-1,2,3,4-tetrahydroacridine hydrochloride (tacrine) and tetraidopropylpyrophosphoramide (iso-OMPA) and a selective AChE inhibitor, donepezil, on the cholinesterase activity in the brain and plasma of rats [33].
• Neither NIK-247 nor THA affected the activity of choline acetyltransferase (ChAT) [34].
• The IL6 genotype may act as a predisposing factor for tacrine transaminitis [35].

Analytical, diagnostic and therapeutic context of Romotal

• These electron microscopy data suggest that tetrahydroaminoacridine treatment results in severe ribosomal dysfunction [12].
• Treatment of Alzheimer's disease with short- and long-term oral THA and lecithin: a double-blind study [36].
• It has been shown in the majority of clinical trials that cholinesterase inhibitors, such as tacrine (tetrahydroaminoacridine), are able to induce beneficial effects in cognition and memory [37].
• Systemic administration of tetrahydroaminoacridine at 1 or 3 mg/kg, i.p., ameliorated the memory deficits and EEG slowing induced by the basal forebrain lesion [38].
• We used Northern blot hybridization to determine whether 9-amino-1,2,3,4-tetrahydroacridine (THA), a potential antidementia drug, selectively altered the levels of muscarinic acetylcholine receptor (mAChR) mRNA in differentiating cerebellar granule cells [39].

References