Single intracerebroventricular administration of amyloid-beta (25–35) peptide induces impairment in short-term rather than long-term memory in rats

Stepanichev, M. Yu.; Moiseeva, Yu. V.; Лазарева, Н. А.; Онуфриев, М. В.; Gulyaeva, N. V.

doi:10.1016/s0361-9230(03)00118-7

Cited by 102 publications

(71 citation statements)

References 50 publications

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“…Aβ (25-35) preferentially impairs spatial and non-spatial short-term memory, and these effects remain evident up to 6 months after even a single i.c.v. injection of the peptide (Stepanichev et al, 2003). In the present work, memory impairment in the passive avoidance test was also confirmed in mice 7 days after the i.c.v.…”

Section: Discussionsupporting

confidence: 82%

Inhibitory Effect of an Ethanol Extract Mixture of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix on Amyloid β Protein (25-35)-Induced Neurotoxicity

Jang

Seong²

2014

Korean Journal of Medicinal Crop Science

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: The present study investigated an ethanol extract (SSB) of a mixture of three medicinal plants of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix for possible neuroprotective effects on neurotoxicity induced by Amyloid β protein (Aβ) (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) . From these results, it is suggested that antidementia effect of SSB is due to its neuroprotective effect against Aβ (25-35)-induced neurotoxicity and that SSB may have a therapeutic role in preventing the progression of Alzheimer's disease.

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Section: Discussionsupporting

confidence: 82%

Inhibitory Effect of an Ethanol Extract Mixture of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix on Amyloid β Protein (25-35)-Induced Neurotoxicity

Jang

Seong²

2014

Korean Journal of Medicinal Crop Science

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“…The compound induced a bell shaped but significant prevention of Ab 25-35 -induced learning deficits, with an active dose about 100 mg/kg. At the morphological level, Ab 25-35 induced a limited but significant cell loss in the CA1 pyramidal cell layer of the hippocampus (Stepanichev et al, 2004) and a marked inflammation in corticolimbic structures that could be visualized by analyzing the GFAP immunolabeling in reactive astrocytes (Stepanichev et al, 2003;Klementiev et al, 2007). Interestingly, although a significant cell loss could be measured in particularly vulnerable areas, like CA1 in mice, GFAP immunolabeling increased in a more diffuse manner, in structures associated with the amyloid deposits, as observed in the retrospenial granular basal cortex and oriens layer of the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

Villard

Espallergues

Keller

et al. 2008

Neuropsychopharmacol

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The antiamnesic and neuroprotective activities of the new aminotetrahydrofuran derivative tetrahydro-N,N-dimethyl-5,5-diphenyl-3-furanmethanamine hydrochloride (ANAVEX1-41), a nonselective muscarinic receptor ligand and s 1 protein activator, were examined in mice injected intracerebroventricularly with amyloid b [25][26][27][28][29][30][31][32][33][34][35] ) peptide (9 nmol). Ab 25-35 impaired significantly spontaneous alternation performance, a spatial working memory, and passive avoidance response. When ANAVEX1-41 (1-1000 mg/kg i.p.) was administered 7 days after Ab 25-35 , ie, 20 min before the behavioral tests, it significantly reversed the Ab 25-35 -induced deficits, the most active doses being in the 3-100 mg/kg range. When the compound was preadministered 20 min before Ab 25-35 , ie, 7 days before the tests, it prevented the learning impairments at 30-100 mg/kg. Morphological analysis of corticolimbic structures showed that Ab 25-35 induced a significant cell loss in the CA1 pyramidal cell layer of the hippocampus that was prevented by ANAVEX1-41 (100 mg/kg). Increased number of glial fibrillary acidic protein immunopositive cells in the retrosplenial cortex or throughout the hippocampus revealed an Ab 25-35 -induced inflammation that was prevented by ANAVEX1-41. The drug also prevented the parameters of Ab 25-35 -induced oxidative stress measured in hippocampus extracts, ie, the increases in lipid peroxidation and protein nitration. ANAVEX1-41, however, failed to prevent Ab 25-35 -induced caspase-9 expression. The compound also blocked the Ab 25-35 -induced caspase-3 expression, a marker of apoptosis. Both the muscarinic antagonist scopolamine and the s 1 protein inactivator BD1047 prevented the beneficial effects of ANAVEX1-41 (30 or 100 mg/kg) against Ab 25-35 -induced learning impairments, suggesting that muscarinic and s 1 targets are involved in the drug effect. A synergic effect could indeed account for the very low active doses measured in vivo. These data outline the therapeutic potential of ANAVEX1-41 as a neuroprotective agent in Alzheimer's disease.

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“…Reversible effects were also reported in an animal model by Holscher et al [7], who found that three daily ICV injections of soluble Aβ (25-35) produced short-and long-term memory impairment in rats tested in a radial-arm maze on post-injection days 12-20, but not on post-injection days 3-11 or 20-28. The difference in the time-course of effects with soluble synthetic Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) and with oligomers of naturally derived Aβ(1-42) from 7PA2 cells is noteworthy and merits investigation with respect to mechanism. Western blot of CM from 7PA2 ( 7 ) and CHO-( C ) cells using antibody 6E10 against the amyloid-β peptide.…”

Section: Discussionmentioning

confidence: 99%

Oligomers of the amyloid-β protein disrupt working memory: Confirmation with two behavioral procedures

Poling

Morgan-Paisley

Panos

et al. 2008

Behavioural Brain Research

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Converging lines of evidence suggest that oligomers of amyloid-β play a role in the cognitive impairment characteristic of Alzheimer's disease, but only three studies have provided experimental evidence of such impairment. To provide additional information about the effects of these oligomers on memory, the present study examined the memory of groups of rats exposed to ICV injections of the culture media (CM) of Chinese Hamster Ovary cells that were (7PA2) and were not (CHO-) transfected with a human mutation of amyloid precursor protein that appears to cause early-onset Alzheimer's disease. The 7PA2 CM, which contained concentrations of soluble amyloid-β oligomers physiologically relevant to those found in human brain, significantly disrupted working memory in rats tested in a radial-arm maze. In contrast, CHO-CM, which did not contain such oligomers, had no effect on memory. The disruptive effects of 7PA2-derived amyloid-β oligomers, evident two hours after exposure, disappeared within a day. These findings are compared to results from 7PA2 CM tested under a complex procedure thought to measure aspects of executive function. The results confirm the disruptive effects of low-n amyloid-β oligomers and extend them to a well established rat model of memory.

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Single intracerebroventricular administration of amyloid-beta (25–35) peptide induces impairment in short-term rather than long-term memory in rats

Cited by 102 publications

References 50 publications

Inhibitory Effect of an Ethanol Extract Mixture of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix on Amyloid β Protein (25-35)-Induced Neurotoxicity

Inhibitory Effect of an Ethanol Extract Mixture of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix on Amyloid β Protein (25-35)-Induced Neurotoxicity

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

Oligomers of the amyloid-β protein disrupt working memory: Confirmation with two behavioral procedures

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