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Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
University of Tehran Medical Science.
Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0002-1342-369X
Shahed University.
2011 (English)In: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 95, no 3, 270-276 p.Article in journal (Refereed) Published
Abstract [en]

Alzheimers disease (AD) is a debilitating neurodegenerative disorder characterized by increased beta-amyloid (A beta) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease in women also suggests a role for estrogen in development of AD. In the present study, effects of the phytoestrogen genistein (10 mg/kg) on learning and memory impairments was assessed in intrahippocampal A beta((1-40))-injected rats. The estrogen receptor antagonist fulvestrant was injected intracerebroventricularly in a group of A beta-lesioned rats. The A beta-injected animals exhibited the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in the RAM task. Genistein, but not genistein and fulvestrant, significantly improved most of these parameters. Measurements of oxidative stress markers in hippocampal tissue of A beta-injected rats showed an elevation of malondialdehyde (MDA) and nitrite content, and a reduction of superoxide dismutase (SOD) activity. Genistein significantly attenuated the increased MDA content but did not affect the nitrite content or SOD activity. These results indicate that genistein pretreatment ameliorates A beta-induced impairment of short-term spatial memory in rats through an estrogenic pathway and by inducing attenuation of oxidative stress.

Place, publisher, year, edition, pages
Elsevier Science B.V., Amsterdam , 2011. Vol. 95, no 3, 270-276 p.
Keyword [en]
Alzheimers disease, Beta-amyloid, Genistein, Learning and memory
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-67550DOI: 10.1016/j.nlm.2010.12.001ISI: 000288774300006OAI: oai:DiVA.org:liu-67550DiVA: diva2:411256
Note
Original Publication: Maryam Bagheri, Mohammad-Taghi Joghataei, Simin Mohseni and Mehrdad Roghani, Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease, 2011, NEUROBIOLOGY OF LEARNING AND MEMORY, (95), 3, 270-276. http://dx.doi.org/10.1016/j.nlm.2010.12.001 Copyright: Elsevier Science B.V., Amsterdam http://www.elsevier.com/Available from: 2011-04-18 Created: 2011-04-18 Last updated: 2016-02-29Bibliographically approved
In thesis
1. Neuroprotective Effect of Genistein: Studies in Rat Models of Parkinson’s and Alzheimer’s Disease
Open this publication in new window or tab >>Neuroprotective Effect of Genistein: Studies in Rat Models of Parkinson’s and Alzheimer’s Disease
2012 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Parkinson’s disease (PD) and Alzheimer’s disease (AD) are neurodegenerative disorders that mainly affect the elderly population. It is believed that oxidative stress is involved in development of both these diseases and that estrogen deficiency is a risk factor for development of AD. Genistein is a plant-derived compound that is similar in structure to estrogen and has anti-oxidative properties. The general objective of the present research was to evaluate the effects of genistein on neurodegeneration in rat models of PD and AD.

Using a rat model of PD, we found that a single intraperitoneal dose of genistein 1 h before intrastriatal injection of 6-hydroxydopamine (6-OHDA) attenuated apomorphine-induced rotational behavior and protected the neurons of substantia nigra pars compacta against 6-OHDA toxicity.

To produce an animal model of AD, we injected Aβ1–40 into the hippocampus of rats. Using groups of these Aβ1–40-lesioned animals, the involvement of estrogen receptors (ERs) was evaluated by intracerebroventricular injection of the estrogen receptor antagonist fulvestrant, and the role of oxidative stress was studied by measuring levels of malondialdehyde (MDA), nitrite, and superoxide dismutase (SOD) activity. The results showed that intrahippocampal injection of Aβ1–40 caused the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in a radial arm maze (RAM task), elevated levels of MDA and nitrite, and a signiHcant reduction in SOD activity in the brain tissue. Furthermore, hippocampus in theses rats exhibited Aβ1–40 immunoreactive aggregates close to the lateral blade of the dentate gyrus (DGlb), extensive neuronal degeneration in the DGlb, high intracellular iNOS+ and nNOS+ immunoreactivity, and extensive astrogliosis.

Genistein pretreatment ameliorated the Aβ-induced impairment of short-term spatial memory, and this effect occurred via an estrogenic pathway and through attenuation of oxidative stress. Genistein also ameliorated the degeneration of neurons, inhibited the formation of Aβ1–40-positive aggregates, and alleviated Aβ1–40-induced astrogliosis in the hippocampus.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2012. 72 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1288
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-77173 (URN)978-91-7519-984-9 (ISBN)
Public defence
2012-06-04, Berzeliussalen, Hälsouniversitetet, Campus Valla, Linköpings universitet, Linköping, 13:00 (English)
Opponent
Supervisors
Available from: 2012-05-07 Created: 2012-05-07 Last updated: 2016-02-29Bibliographically approved

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