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РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.50

Use of phosphatidylserine in sporadic and familial Alzheimer's disease [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / L. Bracco [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P123 . - ISSN 0197-4580
Перевод заглавия: Использование фосфатидилсерина при спорадической и наследственной болезни Алцгеймера
Аннотация: Evolution of the real activity of a drug requires numerous and extensive investigations. Obtaining valid results from clinical trials on dementia depends on two principal factors: the correct diagnosis of the disease underling the dementia syndrome, and the detection of specific cognitive and behavioral disturbance using neuropsychologic measures minimally influenced by different factors. Finally an important aspect of clinical trials on dementia, mainly AD, is the identification of specific outcomes of treatment and subgroups. In fact several factors such as age of onset, familiarity and specific neuropsychological features could effect the course of the disease. The results observed in our double-blind randomized placebo-controlled clinical trial suggest that oral intake of phosphatidylserine (PS) may improve performance on selected cognitive variables as well as prevent further cognitive deterioration in AD patients. Moreover we carried out clinical trials on AD patients taking into consideration the possibility that familial AD patients could respond to PS treatment in a different way respect to sporadic cases. We have also studied the effect of phosphatidylserine (PS) on oxygen metabolite toxicity in skin fibroblast cell lines from apparently normal subjects and from patients with familial and sporadic AD. Fibroblast damage was produced by the generation of oxygen metabolites during the enzymatic oxidation of acetaldehyde by xanthine-oxidase (X-O). In order to quantify cell damage, we measured lactate dehydrogenase (LDH) activity in culture medium and cell viability in fibroblast cultures, with and without preincubation with PS, after X-O incubation. We found a significant increase of LDH activity in cells without PS preincubation, providing evidence of the free radicals damage. No significant increase of LDH activity was observed in the same ce cell lines from normal subjects as well as from patients with familial and sporadic AD after preincubation with PS. In conclusion our study provided evidence suggesting that PS may protect normal and pathological fibroblasts, namely with familial and sporadic AD free radical damage and may be useful in the treatment of this disease

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
СПОРАДИЧЕСКАЯ
НАСЛЕДСТВЕННАЯ
ФОСФАТИДИЛСЕРИН
МЕТАБОЛИЗМ КИСЛОРОДА
ЛАКТАТДЕГИДРОГЕНАЗА
ФИБРОБЛАСТЫ
ТЕРАПЕВТИЧЕСКИЙ ЭФФЕКТ
БОЛЬНЫЕ

Доп.точки доступа:
Bracco, L.; Falcini, M.; Piersanti, P.; Latorraca, S.; Piacentini, S.; Sorbi, S.; Amaducci, L.

РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.51

Neuropharmacological profile of SR46559A, a muscarinic agonist devoid of cholinergic symptomatology [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / J. P. Kan [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P126 . - ISSN 0197-4580
Перевод заглавия: Нейрофизиологический профиль SR46559A, мускаринового агониста, лишенного холинергической симптоматики
Аннотация: Numerous studies support the involvement of central cholinergic systems in learning and memory. In addition, a dramatic loss of presynaptic cholinergic markers has been reported in brains of patients suffering from Alzheimer's disease (AD). Consequently, enhancing cholinergic function has appeared as the main approach to improve cognitive deficits seen in AD. However, clinical trials with acetylcholinesterase (AChE) inhibitors and muscarinic agonists have led to inconclusive results, partly due to incidence of cholinergic side - effects and toxicity. This problem could be circumvented by the discovery of selective muscarinic M[1] receptor agonists. The cholinergic activities of SR 46559A, 3-(N-(2-diethyl-amino-2-methylpropyl)-6-phenyl-5-propyl) pyridazinamine have been investigated in vtiro and in vivo, in rodents. Using rat brain cortical membranes, SR 46559A was a competitive ligand (Ki 112 nM) at muscarinic M[1] receptors, its affinity for muscarinic M[2] (cardiac) and M[3] (glandular) receptors being 6-7 times lower. SR 46559A did not interact with brain nicotinic receptors, high affinity choline uptake sites and AChE. Up to 1 mM, SR 46559A, slightly and inconsistently stimulated inositol phospholipids breakdown and did not inhibit the forskolin-induced activation of adenylyl cyclase activity. However, like muscarinic agonists, SR 46559A inhibited (IC[50] 10 'мю'M) the K{+}-evoked release of ({3}H)GABA from rat striatal slices and reduced at 0.5 and 1 'мю'M, the population spike amplitude of the CA[1] pyramidal cells induced by stimulation of the Schaffer's collateral commissural pathway in rat hippocampal slices. In mice, up to sub-lethal doses, SR 46559A did not induce the typical cholinergic syndrom. Like muscarinic agonists, SR 46559A (0.1 mg/kg PO) potentiated haloperidol-induced catalepsy in rats and antagonized (ED[50]=0.12 mg/kg PO) rotations induced in mice by intrastriatal injection of pirenzepine. SR 46559A antagonized the scopolamine- or pirenzepine-induced deficit in passive avoidance leaming. (ED[50]s=0.25 and 0.027 mg/kg PO, respectively). Moreover, using the social memory test, SR 46559A (0,1-3 mg/kg PO) enhanced short-term retention in adult rats and improved memory deficits observed in aged mice and in rats subjected to cerebral ischemic insult, SR 46559A (1-3 mg/kg PO) also reversed the ischemia-induced alterations of rat's exploratory behaviour. These results suggest that SR 46559A behaves as a partial M[1] muscarinic agonist with marked ability to improve experimentally induced cognitive deficits in rodents without producing cholinergic symptomotalogy. Thus SR 46559A could be a potential useful drug for the symptomatic treatment of AD

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
SR46559A
МЕХАНИЗМ ДЕЙСТВИЯ
ПОКАЗАНИЯ К ПРИМЕНЕНИЮ
IN VITRO
IN VIVO

Доп.точки доступа:
Kan, J.P.; Heaulme, M.; Michaud, J.C.; Olliero, D.; Bolgegrain, R.; Soubrie, P.

РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.52

Does chronic oral physostigmine alter the course of Alzheimer's disease? [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / P. Storey [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P126 . - ISSN 0197-4580
Перевод заглавия: Длительный прием внутрь физостигмина изменяет ли течение болезни Алцгеймера?
Аннотация: There has been renewed interest in the use of cholinesterase inhibitors for the symptomatic treatment of Alzheimer's disease (AD). Although early studies questioned the effectiveness of this therapy, more recent investigations have demonstrated short-term benefit in some AD patients. Moreover, some studies have suggested long-term benefit in that disease progression has been reported to be slowed. These latter studies, however, suffer from small patient number (usually 10) and lack of controls. We sought to re-address this issue by investigating the effects of physostigmine on neuropsychological test performance in a larger number of AD patients and comparing this to a non-treated group of AD patients. Twenty-seven probable AD patients (NINCDS-ADRDA criteria) entering and outpatient trial of oral chronic physostigmine underwent dose finding, double-blind crossover, followed by chronic therapy with the highest tolerated dose (13.2 mg/day). Baseline and yearly neuropsychological assessment was performed with the following battery: Mattis Dementia Rating Scale; Intelligence (WAIS-subscale, Peabody Picture Vocabulary); Attention and Concentration (Wechsler Memory-R attention subscale, Trails A. B.); Language (Boston Naming, Controlled Oral Fluency); Perception (Benton Visual Form Discrimination, Tactile Form Recognition); Motor (Finger Tapping, Grooved Pegs); Memory (Wechsler Memory-R; Selective Reminding. Control probable AD (NINCDS-ADRDA) patients (n

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
ФИЗОСТИГМИН
ДОЗЫ
ТЕРАПЕВТИЧЕСКИЙ ЭФФЕКТ
НЕЙРОФИЗИОЛОГИЧЕСКИЕ ПОКАЗАТЕЛИ
БОЛЬНЫЕ

Доп.точки доступа:
Storey, P.; Harrell, L.; Duke, L.; Callaway, R.; Marson, D.

РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.53

Adem, Abdu.
Putative mechanisms of action of tacrine in Alzheimer's disease [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / Abdu Adem // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P124 . - ISSN 0197-4580
Перевод заглавия: Предполагаемый механизм действия такрина при болезни Алцгеймера
Аннотация: Recently, THA in combination with lecithin was reported to improve cognitive function in patients who had Alzheimer's disease (AD). One possible mechanism for the cognitive improvement in AD patients could be the increase of acetylcholine in their brain tissue by inhibition of cholinesterase enzymes. However, the improved cognitive function may not be entirely due to cholinesterase inhibition. A second possible mechanism could be the direct effect of THA on muscarinic and nicotinic receptors since THA was found to interfere with binding of muscarinic and nicotinic ligands to their receptors. Moreover, THA was reported to inhibit carbachol-stimulated PI hydrolysis at concentrations of 10{-5} and 10{-4} M, which is in accordance with the ability of THA to displace muscarinic ligand binding. In addition to its multiple effects on the cholinergic system, THA has also been reported to have effects on other neurotransmitter systems such as inhibition of monoamine oxidase and inhibition of dopamine and serotonin uptake. These latter effects of THA might be possible mechanisms for improvement of some symptoms of AD. Several studies confirm that THA influences different types of voltage-gated K{+} channels as well as Na{+} and Ca{2+} channels. Thus, a possible mechanism of action of THA could be the blocking of potassium (K{+}) channels or other voltage-dependent monovalent ion channels. The multiple mechanisms of action of THA, all or in part, may contribute to amelioration of some of the symptoms of AD

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
ТАКРИН
МЕХАНИЗМ ДЕЙСТВИЯ
ИНГИБИРОВАНИЕ ХОЛИНЭСТЕРАЗЫ
МУСКАРИНОВЫЕ РЕЦЕПТОРЫ
НИКОТИНОВЫЕ РЕЦЕПТОРЫ
БЛОКАДА КАЛИЕВЫХ КАНАЛОВ
БОЛЬНЫЕ

РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.54

Phosphatidylserine in the treatment of cognitive degline of elderly patients [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / T. Bertoldin [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P126-127 . - ISSN 0197-4580
Перевод заглавия: Фосфатидилсерин при лечении снижения умственной деятельности при старческом слабоумии
Аннотация: Phosphatidylserine, a pharmacologically active phospholipid, has been shown to enhance the activities of membrane-bound enzymes involved in neurotransmitter release and signal transduction in the CNS. Clinical trials with phosphatidylserine have reported positive effects on the cognitive impairment and behavioral disturbances in elderly patients with mild to severe cognitive decline due to various etiologies, including Alzheimer's diseases. However, these trials have usually dealt with small groups of patients selected for the presumptive presence of senile dementias. In this double-blind study the therapeutic effects and the safety of orally treatment with phosphatidylserine vs placebo (300 mg/die for 6 months) was asseassed in a group of geriatric patients with cognitive impairment. A total of 494 elderly patients (age between 65 and 93 yrs), affected by moderate to severe cognitive decline according to the Mini Mental State Examination and Global Deterioration Scale, were recruited in 23 Geriatric or General Medicine Units is Northeastern Italy. Patients were examined just before starting the therapy, and 3 and 6 months thereafter. The efficacy of treatment compared with placebo was measured on the basis of changes occurring in behavior and cognitive performance using the Plutchik Geriatric Rating Scale and the Buschke Selective Reminding Test. Statistically significant improvements in the phosphatidylserine-treated group compared with placebo were observed both in terms of behavioral and cognitive parameters. Clinical evaluation and laboratory tests demonstrated that phosphatydilserine was well tolerated. These results are particular relevance in the light of the large number of patients enrolled in this study, who represent a sample of the geriatric population commonly encountered in clinical practice

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
ФОСФАТИДИЛСЕРИН
ДОЗЫ
ПРОДОЛЖИТЕЛЬНОСТЬ ЛЕЧЕНИЯ
ТЕРАПЕВТИЧЕСКИЙ ЭФФЕКТ
БОЛЬНЫЕ ПОЖИЛЫЕ

Доп.точки доступа:
Bertoldin, T.; Farina, C.; Genacchi, T.; Grepaldi, G.

РЖ ВИНИТИ 76 (BI31) 95.09-04Т3.56

The effects of alpha-glycerylphosphorylcholine administration on the GH secretion of elderly subjects and of patients affected by senile dementia of the Alzheimer type [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / G. P. Ceda [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P126 . - ISSN 0197-4580
Перевод заглавия: Эффекты применения альфа-глицерилфосфорилхолина на секрецию гормона роста у пожилых людей и больных старческим слабоумием по алцеймеровскому типу
Аннотация: GH secretion is blunted during aging in rodents and humans. Central cholinergic stimuli increase the secretion of GH from the pituitary; drugs like the cholinesterase inhibitor pyridostigmine induce GH release, potentiate the stimulatory effect of GHRH and restore the GH response after intermittent GHRH administration. These actions may be mediated by a decrease of somatostatin release. Since brain acetylcholine (Ach) synthesis declines with aging and in dementia, it may be possible to restore normal GH secretion by enhancing cholinergic tone. The putative Ach precursor, alphaglycerylphosphorylcholine (alpha-GFC), has been used for the treatment of amnestic and cognitive disorders of aging. In order to learn what effect alpha-GFC had on GH secretion, GHRH was given to young and old human volunteers and to a group of patients affected by SDAT. 8 young (aged 32'+-'1.9), 7 old subjects (aged 80'+-'2 y) and 5 patients affected by SDAT (aged 79'+-'2.1 y) were studied on separate days with 1) a bolus injection of 50 'мю'g GHRH (Geref, Serono) with blood samples taken at - 15 and O min and at 15, 30, 45, 60 and 90 min after the injection, and 2) a 30 min infusion of alpha-GFC (Brezal, Sandoz) (1g in 100 ml saline) followed by a GHRH bolus injection and samples obtained at the same times. The results showed that GH responses to GHRH were greater in the younger than in the older subjects and both groups had a greater GH response to the GHRH+alpha-GFC stimulation than to GHRH alone. However the potentiating effect of alpha-GFC was more pronounced in the elderly subjects. In patients affected by SDAT both GHRH and GHRH+alpha-GFC induced GH responses similar to that observed in the elderly normal subjects. These findings confirm the observation that 1) aged individuals respond less well to GHRH than younger subjects. 20 the pituitary responsiveness to GHRH in patients affected by SDAT is similar to that of normal subjects of comparable age, and document that 3) the enhancing effects of alpha-GFC is greater in normal elderly subjects. These results provide further evidence that increased cholinergic tone enhances GH release

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
ГЛИЦЕРИЛФОСФОРИЛКОЛИН *АЛЬФА-
ТЕРАПЕВТИЧЕСКИЙ ЭФФЕКТ
СРАВНИТЕЛЬНЫЙ АНАЛИЗ
ЗДОРОВЫЕ МОЛОДЫЕ
ЗДОРОВЫЕ ПОЖИЛЫЕ
БОЛЬНЫЕ ПОЖИЛЫЕ

Доп.точки доступа:
Ceda, G.P.; Marzani, G.P.; Piovani, E.; Denti, L.; Banchini, A.; Tarditi, E.; Baggi, F.; Marchini, L.; Valenti, G.

РЖ ВИНИТИ 76 (BI31) 95.11-04Т3.90

Therapeutic strategies in Alzheimer's disease: Results of the neuropsychological studies with L-deprenyl [Text] : abstr. 3rd Int. Conf. Alzheimer's Disease and Relat. Disorders, Abano Terme, July 12-17, 1992 / G. L. Piccinin [et al.] // Neurobiol. Aging. - 1992. - Vol. 13, Suppl. n 1. - P133-134 . - ISSN 0197-4580
Перевод заглавия: Терапевтическая стратегия при болезни Альцгеймера: результаты нейропсихологического исследования с L-депренилом

ГРНТИ	76.31.29

ВИНИТИ 761.31.29.09.21.11
Рубрики: АЛЦГЕЙМЕРА БОЛЕЗНЬ
ДЕПРЕНИЛ * L-
НЕЙРОПСИХОЛОГИЧЕСКИЕ ТЕСТЫ
КЛИНИЧЕСКИЙ ЭФФЕКТ
БОЛЬНЫЕ

Доп.точки доступа:
Piccinin, G.L.; Finali, G.; Piccirilli, M.; Oliani, C.

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