Effects of repeated administration of propentofylline on memory impairment produced by basal forebrain lesion in rats

Fuji, Kazuyuki; Hiramatsu, Masayuki; Kameyama, Tsutomu; Nabeshima, Toshitaka

doi:10.1016/0014-2999(93)90479-2

Cited by 38 publications

(11 citation statements)

References 23 publications

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“…The experimental apparatus consisted of a locomotor cage (25×42×20 cm), with photobeams placed 2 cm above the floor at 1‐inch intervals along two sides of the cage (Colombus Instruments, U.S.A.). Locomotor activity was measured during a 10 min period (Fuji et al ., 1993).…”

Section: Methodsmentioning

confidence: 99%

Long‐term deprivation of oestrogens by ovariectomy potentiates β‐amyloid‐induced working memory deficits in rats

Yamada

Tanaka

Zou

et al. 1999

British J Pharmacology

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1 In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory de®cits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid b-peptide (Ab), the major constituent of senile plaques in AD. 2 Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a signi®cant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3 A continuous i.c.v. infusion of Ab-(1-42) caused spatial learning and memory de®cits in both ovariectomized and sham-operated rats. 4 The Ab-induced working memory de®cits were signi®cantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5 These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory de®cits produced by Ab-(1-42) in rats.

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Section: Methodsmentioning

confidence: 99%

Long‐term deprivation of oestrogens by ovariectomy potentiates β‐amyloid‐induced working memory deficits in rats

Yamada

Tanaka

Zou

et al. 1999

British J Pharmacology

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“…for 211 d starting 8 d after the induction of lesions) significantly reversed the compensatory increase in muscarinic binding sites and binding affinity in the frontal and parietal cortex and the hippocampus of rats with basal forebrain lesions induced by ibotenic acid (1 9). In a separate study using the same experimental model and dosing regimen, propentofylline prevented a decrease in choline acetyltransferase activity in the hippocampus but not in the cortical areas (20). Since the ibotenic acid lesion does not selectively destroy cholinergic neurons, the improvement in learning and memory elicited by propentofylline may also be due to a reduction of non-cholinergic brain dysfunction.…”

Section: Learning and Memorymentioning

confidence: 96%

Propentofylline (HWA 285), a Neuroprotective Glial Cell Modulator: Pharmacologic Profile

Rudolphi¹,

Park

Rother³

1997

CNS Drug Reviews

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“…Propentofylline (Hextol™), a xanthine derivative with both adenosine uptake inhibitor properties [242] and A 1 adenosine receptor antagonist properties [243], increases the production and secretion of NGF from cultured astrocytes [244] as well as increasing the production of NGF in animal models of dementia [245]. Propentofylline is neuroprotective in several models of neurodegeneration and ischaemia [246,247], and reverses the deficits of learning and memory produced by the infusion of β-amyloid into the brain [248]. Propentofylline has shown promise in clinical trials for treatment of both AD and cerebrovascular dementia, producing significant improvements in both cognitive performance and in metabolic measurements [249][250][251].…”

Section: Neurotrophic Factors and Oestrogenmentioning

confidence: 99%

Emerging strategies for the treatment of Alzheimer’s disease at the Millennium

Emmerling¹,

Spiegel²,

Hall³

et al. 1999

Emerging Drugs

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It is estimated that by the year 2050 the number of cases of Alzheimer's disease (AD) will more than triple in the United States alone. As longevity increases, AD cases are expected to skyrocket from 4 -14 m. Globally, the numbers may reach 60 -80 m. Those expected to develop AD in the next century are presently in their 20s, 30s or 40s. Thus, steps must be taken to prevent this imminent epidemic, and the emotional and economic toll that it will exact on both patients and families. Numerous new strategies to treat AD have emerged in the last decade. This is the direct result of an increased understanding of the molecular pathology associated with the development of AD dementia, as well as the harvesting of results from case-control and cohort epidemiological studies. AD is no longer viewed solely as a disease of neurotransmitter deficits or amyloid deposition. Rather, it is a combination of events (amyloidosis, neurofibrillary pathology, inflammation, oxidative stress and cerebral vascular insufficiency) that conspire to produce this dementia. This avalanche of information reveals the complexity of the genetic and environmental contributors to AD. At the same time, these advances also delineate new avenues by which AD may be palliated, halted or averted. In the present review, we shall explore the emerging opportunities for the treatment and prevention of AD. 35 1999

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Effects of repeated administration of propentofylline on memory impairment produced by basal forebrain lesion in rats

Cited by 38 publications

References 23 publications

Long‐term deprivation of oestrogens by ovariectomy potentiates β‐amyloid‐induced working memory deficits in rats

Long‐term deprivation of oestrogens by ovariectomy potentiates β‐amyloid‐induced working memory deficits in rats

Propentofylline (HWA 285), a Neuroprotective Glial Cell Modulator: Pharmacologic Profile

Emerging strategies for the treatment of Alzheimer’s disease at the Millennium

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