Molecular strategies for the first generations of antidementia drugs. (I). Tacrine and related compounds

Cacabelos, Ramón; Nordberg, A.; Caamaño, J.

doi:10.1358/dot.1994.30.4.287372

Cited by 34 publications

(33 citation statements)

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“…Improvement of learning in animals with impaired cognitive functions resulting from disturbances in the cen- 10 (91) tral nervous system of various origin or in animals with scopolamine-induced amnesia treated with tacrine was described by other researchers [7]. We previously observed this effect of tacrine in animals treated with high doses of AF64A [14].…”

Section: Resultsmentioning

confidence: 58%

“…In this work we used tacrine as a reference drug because of its ability to improve TWAA acquisition. The cognitive effects of tacrine have been initially explained by its anticholinesterase activity; further investigations showed that this drug exhibits a broad spectrum of biochemical and physiological effects [7]. However, the mechanisms underlying the positive effect of tacrine on cognitive functions under pathological conditions are poorly studied.…”

Section: Resultsmentioning

confidence: 99%

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Dimebon improves learning in animals with experimental Alzheimer's disease

et al. 2000

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Section: Resultsmentioning

confidence: 58%

Section: Resultsmentioning

confidence: 99%

Dimebon improves learning in animals with experimental Alzheimer's disease

et al. 2000

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“…phvsostigmine infusion produced significant improvement which correlated with rCBF changes [82], It has also been uti lized in trials with oral tetrahydroaminoacridine [83,84], The pretreatment EEG as well as drug effect on EEG dif fered in clinical responders and nonresponders. Electrophysiologic brain mapping has also been found useful in trials in DAT patients with CDP-choline [85], and several nootropic drugs [72]. The effect on quantitative EEG of single intravenous doses of scopolamine has been suggest ed as a test of the degree of cholinergic deficiency in Alz heimer's disease [86], EEG in P ic k 's Disease and Frontal Lobe Dem entias EEG in patients with histologically verified frontotem poral cortical atrophy were found to be normal or moder ately abnormal despite prolonged dementia of increasing severity [37,68].…”

Section: Differentiation Between D a T And Cerebrovascular Dementiamentioning

confidence: 99%

Electroencephalography as a Diagnostic Tool in Dementia

Rosén

1997

Dement Geriatr Cogn Disord

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Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse β activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.

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“…1995 of nicotine receptors and to a lesser degree reduction in muscarinic receptors have been seen [7]. Acetylcholine is involved in memory' and other cognitive processes [8].…”

Section: Introductionmentioning

confidence: 99%

“…The degeneration of cholinergic pathways in AD corre lates with the degree of dementia [9]. Therefore, a large number of clinical trials have aimed at enhancing cholin ergic transmission by treatment with precursors, agonists or AChE inhibitors such as physostigmine and tetrahydroaminoacridine (tacrine) [7,[10][11][12][13],…”

Section: Introductionmentioning

confidence: 99%

Long-Term Effects of Tacrine on Regional Cerebral Blood Flow Changes in Alzheimer’s Disease

Minthon

Nilsson²,

Edvinsson

et al. 1995

Dement Geriatr Cogn Disord

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Regional cerebral blood flow (rCBF) was studied in patients with Alzheimer''s disease (AD) before and after 14 months of tacrine treatment. The treated group was compared with an identical reference group of untreated AD patients. At baseline the two groups showed an identical rCBF and mean hemispheric blood flow. After 14 months the tacrine-treated patients showed a stable rCBF level and a signiflcant increase in rCBF in the central-parietal regions, compared to the untreated reference group, who showed typical AD reductions in rCBF in these regions. Clinical outcome: 7 of 9 patients in the tacrine group were clinically unchanged or slightly improved during the study time. In the untreated group 8 of 11 patients had deteriorated in clinical assessments and none had improved. Long-term tacrine treatment in Alzheimer''s disease may delay the progression of symptoms.

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Molecular strategies for the first generations of antidementia drugs. (I). Tacrine and related compounds

Cited by 34 publications

References 0 publications

Dimebon improves learning in animals with experimental Alzheimer's disease

Dimebon improves learning in animals with experimental Alzheimer's disease

Electroencephalography as a Diagnostic Tool in Dementia

Long-Term Effects of Tacrine on Regional Cerebral Blood Flow Changes in Alzheimer’s Disease

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