Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine
Environmental factors including chronic stress may play a critical role in the manifestation of Alzheimer’s disease (AD).This review summarizes our studies of the aggravation of the impaired cognitive ability and its cellular and molecular correlates by chronic psychosocial stress and prevention by...
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| Format: | Online |
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Bentham Science Publishers
2011
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263455/ |
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pubmed-3263455 |
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pubmed-32634552012-06-01 Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine Alkadhi, Karim A Article Environmental factors including chronic stress may play a critical role in the manifestation of Alzheimer’s disease (AD).This review summarizes our studies of the aggravation of the impaired cognitive ability and its cellular and molecular correlates by chronic psychosocial stress and prevention by nicotine in an Aβ rat model of AD. We utilized three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of the cellular correlates of memory, long-term potentiation (LTP) and long-term depression (LTD), in anesthetized rats, and immunoblot analysis of synaptic plasticity- and cognition-related signaling molecules. The Aβ rat model, representing the sporadic form of established AD, was induced by continuous i.c.v. infusion of a pathogenic dose of Aβ peptides via a 14- day osmotic pump. In this AD model, chronic stress intensified cognitive deficits, accentuated the disruption of signaling molecules levels and produced greater depression of LTP than what was seen with Aβ infusion alone. Chronic treatment with nicotine was highly efficient in preventing the effects of Aβ infusion and the exacerbating impact of chronic stress. Possible mechanisms for the effect of chronic stress are discussed. Bentham Science Publishers 2011-12 /pmc/articles/PMC3263455/ /pubmed/22654719 http://dx.doi.org/10.2174/157015911798376307 Text en ©2011 Bentham Science Publishers http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Alkadhi, Karim A |
| spellingShingle |
Alkadhi, Karim A Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| author_facet |
Alkadhi, Karim A |
| author_sort |
Alkadhi, Karim A |
| title |
Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| title_short |
Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| title_full |
Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| title_fullStr |
Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| title_full_unstemmed |
Chronic Stress and Alzheimer’s Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine |
| title_sort |
chronic stress and alzheimer’s disease-like pathogenesis in a rat model: prevention by nicotine |
| description |
Environmental factors including chronic stress may play a critical role in the manifestation of Alzheimer’s disease (AD).This review summarizes our studies of the aggravation of the impaired cognitive ability and its cellular and molecular correlates by chronic psychosocial stress and prevention by nicotine in an Aβ rat model of AD. We utilized three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of the cellular correlates of memory, long-term potentiation (LTP) and long-term depression (LTD), in anesthetized rats, and immunoblot analysis of synaptic plasticity- and cognition-related signaling molecules. The Aβ rat model, representing the sporadic form of established AD, was induced by continuous i.c.v. infusion of a pathogenic dose of Aβ peptides via a 14- day osmotic pump. In this AD model, chronic stress intensified cognitive deficits, accentuated the disruption of signaling molecules levels and produced greater depression of LTP than what was seen with Aβ infusion alone. Chronic treatment with nicotine was highly efficient in preventing the effects of Aβ infusion and the exacerbating impact of chronic stress. Possible mechanisms for the effect of chronic stress are discussed. |
| publisher |
Bentham Science Publishers |
| publishDate |
2011 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263455/ |
| _version_ |
1611501472270254080 |