Dr. Weeks’ Comment: Black cumin seed is 181x more effective as an anti-inflammatory agent compared to aspirin (Lucy Lu U Maryland) and since Alzheimer’s disease is driven by inflammation, those with memory challenges need to be eating black cumin seeds – and the whole crushed organic non-GMO seeds are vastly superior to extracted seed oil. Here are six studies to reinforce your commitment to enhancing your memory.
“…TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation…”
“…The results of the present study showed that TQ protected against PTU-induced memory impairments in rats…”
“… The evidence presented in this paper appears to be supporting the hypothesis that this plant and/or its bioactive constituents can enhance learning and memory in health and disease in animals…”
1.
Abulfadl YS1, El-Maraghy NN1, Ahmed AE2, Nofal S2, Abdel-Mottaleb Y1, Badary OA3.
Hum Exp Toxicol. 2018 Jan 1:960327118755256. doi: 10.1177/0960327118755256.
Abstract
Alzheimer’s disease (AD) is characterized by a robust inflammatory response elicited by the accumulation and deposition of amyloid-β (Aβ) within the brain. Aβ induces detrimental inflammatory responses through toll-like receptors (TLRs) signaling pathway. Thymoquinone (TQ), the main active constituent of Nigella sativa oil, has been reported by several previous studies for its potent anti-inflammatory effect. The aim of this study is to elucidate the effect of TQ in improving learning and memory, using a rat model of AD induced by a combination of aluminum chloride (AlCl3) and d-galactose (d-Gal). TQ was administered orally at doses of 10, 20, and 40 mg/kg/day for 14 days after AD induction. Memory functions were assessed using the step through passive avoidance test. Amyloid plaques were shown to be present using hematoxylin and eosin staining. Tumor necrosis factor-alpha (TNF-α) and Interleukin-1beta (IL-1β) levels in brain were assessed via ELISA and profiling TLR-2, TLR-4, myeloid differential factor 88, toll-interleukin-1 receptor domain-containing adapter-inducing interferon-β, interferon regulatory factor 3 (IRF-3), and nuclear factor-κB (NF-κB) expressions via real-time polymerase chain reaction. TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses ( p < 0.05). We concluded that TQ reduced the inflammation induced by d-Gal/AlCl3 combination. It is therefore reasonable to assign the anti-inflammatory responses to the modulation of TLRs pathway.
2.
Baghcheghi Y1, Hosseini M2, Beheshti F3, Salmani H4, Anaeigoudari A5.
Arq Neuropsiquiatr. 2018 Jan;76(1):32-40. doi: 10.1590/0004-282X20170182.
Abstract
In this study, the effect of thymoquinone (TQ) on propylthiouracil (PTU)-induced memory impairment was investigated in juvenile rats. The rats were grouped into control, Hypo, Hypo-TQ5 and Hypo-TQ10. Propylthiouracil increased latency time in the Morris water maze test and decreased delay in entering the dark compartment in the passive avoidance test. Both 5 mg/kg and 10 mg/kg doses of TQ decreased latency time in the Morris water maze test and increased delay in entering the dark compartment in a passive avoidance test. The PTU also increased malondialdehyde and nitric oxide metabolites in the brain while reduced the thiol content and superoxide dismutase and catalase activities and serum T4 level. Both doses of TQ decreased malondialdehyde and nitric oxide metabolites in the brain while enhanced the thiol content and superoxide dismutase and catalase activities and serum T4 level. The results of the present study showed that TQ protected against PTU-induced memory impairments in rats.
3.
Bargi R1, Asgharzadeh F2, Beheshti F3, Hosseini M4, Sadeghnia HR5, Khazaei M2.
Cytokine. 2017 Aug;96:173-184. doi: 10.1016/j.cyto.2017.04.015. Epub 2017 Apr 19.
OBJECTIVE:
The study objective was to determine the protective effects of thymoquinone (TQ) on brain tissues oxidative stress status, hippocampal cytokine level, and learning and memory deficits induced by lipopolysaccharide (LPS) in rats.
CONCLUSION:
Findings of current study indicated that TQ improved LPS-induced learning and memory impairments induced by LPS in rats by attenuating the hippocampal cytokine levels and brain tissues oxidative damage.
4.
Shao YY1, Li B2, Huang YM1, Luo Q1, Xie YM1, Chen YH1.
Transl Neurosci. 2017 Mar 25;8:9-14. doi: 10.1515/tnsci-2017-0003. eCollection 2017 Jan.
AIM:
Status epilepticus (SE) results in the generation of reactive oxygen species (ROS), which contribute to seizure-induced brain injury. It is well known that oxidative stress plays a pivotal role in status epilepticus (SE). Thymoquinone (TQ) is a bioactive monomer extracted from black cumin (Nigella sativa) seed oil that has anti-inflammatory, anti-cancer, and antioxidant activity in various diseases. This study evaluated the protective effects of TQ on brain injury in a lithium-pilocarpine rat model of SE and investigated the underlying mechanism related to antioxidative pathway.
RESULTS:
Latency to SE increased in the TQ-pretreated group compared with rats in the model group, while the total power was significantly lower. Seizure severity measured on the Racine scale was significantly lower in the TQ group compared with the model group. Results of behavioral experiments suggest that TQ may also have a protective effect on learning and memory function. Investigation of the protective mechanism of TQ showed that TQ-pretreatment significantly increased the expression of Nrf2, HO-1 proteins and SOD in the hippocampus.
CONCLUSION:
These findings showed that TQ attenuated brain injury induced by SE via an anti-oxidative pathway.
5.
Abdel-Zaher AO1, Farghaly HSM2, Farrag MMY2, Abdel-Rahman MS2, Abdel-Wahab BA2.
Biomed Pharmacother. 2017 Apr;88:553-561. doi: 10.1016/j.biopha.2017.01.009. Epub 2017 Jan 25.
Abstract
Cognitive dysfunction is commonly observed in epileptic patients. Pentylenetetrazole (PTZ) kindling is a well established animal model which simulates clinical epilepsy. This study evaluated the potential role of glutamate, oxidative stress and nitric oxide (NO) overproduction in pentylenetetrazole (PTZ)-induced kindling and associated cognitive impairments in mice and effect of thymoquinone on these parameters. Repeated treatment of mice with a subconvulsive dose of PTZ (35mg/kg i.p.) once every alternate-day for 12 injections induced kindling. PTZ-kindled mice showed learning and memory impairments as assessed by acquisition and probe trials of Morris water maze and step-through latency of passive avoidance tests. Concurrently, the brain glutamate, malondialdehyde and nitrite levels were increased while the brain intracellular reduced glutathione level and glutathione peroxidase activity were decreased in PTZ-kindled mice. Also, the brain inducible but not neuronal NO synthase mRNA and protein expressions were increased in PTZ-kindled mice. Treatment of mice with thymoquinonne (5, 10 and 20mg/kg i.p.) along with alternate-day subconvulsive dose of PTZ produced dose-dependent protection against PTZ-induced kindling and learning and memory impairments. Moreover, treatment of mice with thymoquinonne (20mg/kg) inhibited the biochemical alterations induced by PTZ in the brain except the elevation of brain glutamate level. The associated increase in brain inducible NO synthase mRNA and protein expressions were also inhibited. These results suggest that glutamate, and subsequent oxidative stress and NO overproduction, via inducible NO synthase, play an important role in the pathophysiology of PTZ-induced kindling and cognitive impairments in mice. Thymoquinone dose-dependently protects against PTZ-induced kindling and cognitive impairments. Inhibition of PTZ-induced brain oxidative stress and NO overproduction, via increase the expression and activity of inducible NO synthase, may play an important role in thymoquinone action.
6.
The Role of Nigella sativa and Its Active Constituents in Learning and Memory.
Sahak MK1, Kabir N1, Abbas G2, Draman S1, Hashim NH3, Hasan Adli DS1.
Evid Based Complement Alternat Med. 2016;2016:6075679. doi: 10.1155/2016/6075679. Epub 2016 Feb 28.
Abstract
The loss of the ability for learning and memory is a prominent feature of dementia, which affects millions of individuals all over the world, due to either neurodegenerative diseases or brain injury. Although a lot of information is known about the pathology involved, treatment remains elusive at best. The Black Seed of Nigella sativa has been historically and religiously used for thousands of years for preventing and treating many different kinds of diseases. This review article looks at Nigella sativa and its potential role in facilitating learning and memory. The possible use of this seed’s extract or compounds isolated from it, such as thymoquinone, for treating damaged brain neural tissue is discussed. The evidence presented in this paper appears to be supporting the hypothesis that this plant and/or its bioactive constituents can enhance learning and memory in health and disease in animals