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Deprenyl, in Alzheimer’s disease

Targum SD, Greenberg RD, Harmon RE, et al Thyroid hormone and the TRH stimulation test in refractory depression. J Chn Psychiatry 45 345-346, 1984 Tariot PN, Cohen RM, Sunderland T L-Deprenyl in Alzheimer s disease. Arch Gen Psychiatry 44 427-433, 1987... [Pg.755]

The first two studies to demonstrate the beneficial effect of (-)-deprenyl in Alzheimer s disease were published in 1987 (Martini et al. 1987 Tariot et al. 1987), and a series of clinical studies with small sample sizes confirmed thereafter the usefulness of this drug in the treatment of the disease (see Knoll 2001, for review). In some of these studies the effect of (-)-deprenyl was compared with other drugs. Campi et al. (1990) found (-)-deprenyl to be... [Pg.92]

Tariot PN, Cohen RM, Sunderland T, et al. L-Deprenyl in Alzheimer s disease. Arch Gen Psychiatry 1987 44 427-433. [Pg.1173]

Schneider LS, Pollock VE, Zemansky MF, et al. A pilot study of low-dose L-deprenyl in Alzheimer s disease. J Geriatr Psychiatry Neurol 1991 4 143-148. [Pg.1173]

The realization of the peculiar effect of (-)-deprenyl, first in Parkinson s disease and later in Alzheimer s disease, distracted attention from its antidepressant property, which remained unutilized. Even an especially interesting aspect of this problem fell into oblivion. In a study performed by Birkmayer et al. (1984) on 102 outpatients and 53 inpatients, (-)-deprenyl was given together with (-)-phenylalanine. The latter is a precursor of PEA that, in contrast to PEA, crosses the blood-brain barrier and, as it is metabolized in the brain, increases the concentration of this natural enhancer substance. Nearly 70% of the patients achieved full remission. This outstanding clinical efficiency was equaled only by that of electroconvulsive treatment, but without the latter s side effect of memory loss. [Pg.88]

It is often stated that early phase studies are impossible in Alzheimer s disease because the corrective action of a truly effective drug on the inevitably long progression of the physiological process would be too slow. On this basis, levodopa, which is so important for Parkinson patients, would still be on the laboratory shelf For the same reason, deprenyl (MAOI-B) - initially developed for its purely symptomatic effect - is now being studied for its possible cytoprotector action [97, 98]. In Alzheimer s disease, there has been discussion (and some efforts at verification) as to whether drugs initially con-... [Pg.31]

The rationale and design of the first multicenter study of (-)-deprenyl in the treatment of Alzheimer s disease using novel clinical outcomes was published by Sano et al. in 1996 and the results of this study were published 1 year later (Sano et al. 1997). The primary outcome involved the time that elapses until the occurrence of any of the following death, institutionalization, loss of the ability to perform basic activities of daily living, or severe dementia. There were significant delays in the time taken for such primary outcomes to occur in patients treated with (-)-deprenyl. The authors concluded that in patients with moderately severe impairment from Alzheimer s disease, treatment with (-)-deprenyl slows the progression of the disease. [Pg.93]

Cytokines, such as tumor necrosis alfa and oxygen radicals, may be produced by HIV-infected macrophages or microglia. These substances cause apoptosis in the cerebral cortex and basal ganglia. Selegiline, also called deprenyl, and thioctic acid are monoamine oxidase-B inhibitors that have antioxidative effects and have been evaluated in tv o clinical hdals. Deprenyl has been previously studied in patients with Alzheimer s dementia and Parkinson s disease, showing improvement of memory in these conditions. [Pg.614]


See other pages where Deprenyl, in Alzheimer’s disease is mentioned: [Pg.665]    [Pg.492]    [Pg.369]    [Pg.153]    [Pg.160]    [Pg.1173]    [Pg.146]    [Pg.156]   
See also in sourсe #XX -- [ Pg.492 ]




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Deprenyl

In Alzheimer’s Disease

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