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| 005 | 20250223032904.0 | ||
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_aEG-GiCUC _beng _cEG-GiCUC |
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| 041 | 0 | _aeng | |
| 049 | _aDeposite | ||
| 097 | _aPh.D | ||
| 099 | _aCai01.08.09.Ph.D.2021.Is.E | ||
| 100 | 0 | _aIsraa Mohamed Abdelfatah Ismail Farag | |
| 245 | 1 | 0 |
_aEffect of dimethyl fumarate on cognitive deficitsin experimentally-induced Alzheimer's disease / _cIsraa Mohamed Abdelfatah Ismail Farag ; Supervised Dalaal Moustafa Abdallah , Hanan Salah Eldin Elabhar , Heba Mohamed Ahmed Ali Abdelrazek |
| 246 | 1 | 5 | _aتأثير ثنائى ميثيل فيوماريت على أختلالات التعرف الناتج عن مرض الزهايمر المحدث تجريبيا |
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_aCairo : _bIsraa Mohamed Abdelfatah Ismail Farag , _c2021 |
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| 300 |
_a129 P. : _bcharts , facsimiles ; _c25cm |
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| 502 | _aThesis (Ph.D.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology | ||
| 520 | _aSince the role of estrogen in postmenauposal-associated dementia is still debatable, this issue urges the search for other medications. Dimethyl fumarate (DMF) is a drug used for the treatment of multiple sclerosis and has shown a neuroprotective effect against other neurodegenerative diseases. Accordingly, the present study aimed to evaluate the effect of DMF on an experimental model of Alzheimer disease (AD) using D-galactose (D-Gal) administered to ovariectomized (OVX) rats, resembling a postmenopausal dementia paradigm. Adult 18-month old female Wistar rats were allocated into sham-operated and OVX/D-Gal groups that were either left untreated or treated with DMF for 56 days starting three weeks after sham-operation or ovariectomy. DMF succeeded to ameliorate cognitive (learning/short- and long-term memory) deficits and to enhance the dampened overall activity (NOR, Barnes-/Y-maze tests).These behavioral upturns were associated with increased intact neurons (Nissl stain) and a reduction in OVX/D-Gal-mediated hippocampal CA1 neurodegeneration and astrocyte activation assessed as GFAP immunoreactivity. Mechanistically, DMF suppressed the hippocampal contents of AD-surrogate markers; viz., apolipoprotein (APO)-E1, BACE1, AÝ42, and hyperphosphorylated Tau. Additionally, DMF has augmented the neuroprotective parameters p-AKT, its downstream target CREB and BDNF. Besides, it activated AMPK, and enhanced SIRT-1, as well as antioxidant defenses (SOD, GSH) | ||
| 530 | _aIssued also as CD | ||
| 653 | 4 | _aAPO-E1 | |
| 653 | 4 | _aBACE1 | |
| 653 | 4 | _aGFAP | |
| 700 | 0 |
_aDalaal Moustafa Abdallah , _eSupervisor |
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| 700 | 0 |
_aHanan Salah Eldin Elabhar , _eSupervisor |
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| 700 | 0 |
_aHeba Mohamed Ahmed Ali Abdelrazek , _eSupervisor |
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| 856 | _uhttp://172.23.153.220/th.pdf | ||
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_aNazla _eRevisor |
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| 905 |
_aShimaa _eCataloger |
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| 942 |
_2ddc _cTH |
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_c83706 _d83706 |
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