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Fenugreek in Management of Neurological and Psychological Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Rohini Pujari, Prasad Thakurdesai
DG has been reported to improve the cognitive deficit in human immunodeficiency virus (HIV) infection-induced dementia mode (in vitro) in human neuronal cultures with E4 allele of Apolipoprotein E (ApoE) (Turchan-Cholewo et al. 2006). The HIV-infected individuals with the E4 allele of Apolipoprotein E (ApoE) or a history of intravenous drug abuse are known to be at risk of developing dementia and peripheral neuropathy (Corder et al. 1998). In vitro studies showed that HIV proteins such as Tat and gp120, Tat + morphine produced increased neurotoxicity in human neuronal cultures with ApoE4 allele with differential alteration of transcripts involved in energy metabolism in cultures of ApoE3 and 4 neurons. DG showed marked neuroprotection against the Tat + morphine-induced neurotoxicity and oxidative stress and impaired morphine metabolism (Turchan-Cholewo et al. 2006). Furthermore, the neuroprotective and memory-enhancing efficacy of DG-rich yam was reported in senescent mice induced by D-galactose (D-gal). DG-rich yam and increased learning and memory abilities of the mice in the Morris water maze test reduced the oxidative stress in the brains of D-gal treated mice (Chiu et al. 2009). These results are further confirmed during a double-blind, placebo-controlled, randomized, crossover clinical study in healthy adults (Tohda et al. 2017).
Role of Vitamin D and Antioxidant Functional Foods in the Prevention and Treatment of Alzheimer’s Disease Pathology
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
There are numerous reports highlighting that dietary supplements of plant and fruit origin such as figs may impact the development of AD. Supplementation given to AD transgenic mice models, APPsw/Tg2576, caused a significant reduction in Aβ peptide levels, the main component of Aβ plaques in both the hippocampus and cortex. ATP levels were also increased with dietary supplementation, suggesting an improvement of cerebral energy production in this model of AD (Essa et al., 2015). Diets rich in figs and fig-leaf extracts potentially affect AChE activity and may have a meaningful impact on disease manifestation. They significantly attenuate oxidative damage with decreased lipid peroxidation, decrease plasma levels of Aβ, and increase antioxidant enzyme activity in both the cortex and hippocampus. After 15 months of administration of a 4% fig diet, improved learning and memory in APPsw/Tg 2576 transgenic mice was observed in cognitive assessment using the Morris water maze test (Subash et al., 2014) (Figure 12.3).
Animal Models of Down Syndrome and Other Genetic Diseases Associated with Mental Retardation
Published in Merlin G. Butler, F. John Meaney, Genetics of Developmental Disabilities, 2019
Angela J. Villar, Charles J. Epstein
Muscatelli et al. (162) produced mice deficient for necdin (Ndn), a gene expressed in postmitotic neurons that possibly plays a role in cell cycle arrest in terminally differentiated neurons. Viable Ndn mutans showed a reduction in both oxytocin-producing and luteinizing hormone-releasing hormone (LHRH)-producing neurons in hypothalamus representing the first evidence of a hypothalamic deficiency in a mouse model of PWS. Although behavioral responses related to motor co-ordination, exploratory activity, anxiety and stress appear unaffected, the mice demonstrated skin scraping activity in the open field test, reminiscent of the skin picking behavior described in PWS patients (162). One of the characteristic strengths of the PWS phenotype is enhanced visual-spatial integration and visual memory, behavioral responses measured by the Morris water maze test. Not surprisingly, Ndn-deficient mice demonstrated improved performance in the Morris water maze suggesting that necdin deficiency may improve cognitive function through changes in neuropeptide levels and/or neurotransmitter activity (162).
Neuroprotective effect of Morin via TrkB/Akt pathway against diabetes mediated oxidative stress and apoptosis in neuronal cells
Published in Toxicology Mechanisms and Methods, 2022
The Morris water maze test was used for the evaluation of spatial learning and memory deficit in the animals. After 30 days of diabetes induction, all diabetic groups in untreated conditions exhibited longer escape latencies throughout the training sessions than the normal rats (Figure 1(A)). It reveals cognitive dysfunction. Then the rats were subjected to morin and metformin treatment for 60 days. At the end of the study, normal healthy groups showed improved performance in the Morris water maze test in four consecutive trials. STZ-induced rats exhibited longer escape latencies throughout training sessions than the normal groups. Oral administration of morin significantly decreased mean latency time at the 3rd and 4th sessions as compared to the 1st session (p < 0.05). Positive control drug metformin administration (100 mg/kg) also reduced the mean latency time significantly. A significant effect was observed in morin-treated DE rats (Figure 1(B)) as compared to metformin-treated DE rats.
Mulberry fruit improves memory in scopolamine-treated mice: role of cholinergic function, antioxidant system, and TrkB/Akt signaling
Published in Nutritional Neuroscience, 2021
Suk Kyung Shin, Jae-Myung Yoo, Fu Yi Li, Seong Yeon Baek, Mee Ree Kim
Morris water maze test was performed according to a method reported previously [3]. Briefly, 1 h before the trial, mice were administrated with MFE (0–200 mg/kg, p.o.) once a day during experimental period. Three weeks after the treatment with MFE, the mice were intraperitoneally administrated with scopolamine (2 mg/kg) for 5 min, and then they were subjected to Morris water maze test for 6 days. On first day, the mice were given to swimming training for 120 s in the absence of the platform. Next, they were given four trial sessions per day with the platform for 4 days. The time interval between each trial session was 20 min. When a mouse located the platform, it was permitted to remain on it for 10 s. If the mouse did not locate the platform within 120 s, it was placed on the platform for 10 s. On final day, the mice were subjected to a probe trial, in which the platform was removed from the water pool, and they were allowed to swim for 120 s to search for the platform. The escape latency time, which taken to cross the platform for the first time, and the number of crossing platform area in 120 s were recorded using a video camera (TGCAM-2000STA, Sambo Electronic Co., Ltd., Korea) connected to the EyeLine Video system.
Protease nexin-1 protects against Alzheimer’s disease by regulating the sonic hedgehog signaling pathway
Published in International Journal of Neuroscience, 2021
Xiao-Long Li, Pu Wang, Yuan Xie
The results of the Morris water maze test are shown in Figure 1. The escape latency of APP/PS1 transgenic AD mice was significantly prolonged, and these mice exhibited a reduced number of platform crossings; these effects were improved by the administration of PN-1 lentiviral activation particles. Thioflavin S staining also indicated that the obvious β-amyloid (Aβ) deposition in APP/PS1 transgenic AD mice was reduced by PN-1 overexpression (Figure 2(A)). Additionally, ELISA analysis revealed that the mice in the APP/PS1 + vector group had the highest level of toxic Aβ1–42 in the hippocampus, followed by those in the APP/PS1 + PN-1 group, while no significant difference was observed between the mice in the WT + vector group and those in the WT + PN-1 group (Figure 2(B)). Moreover, TUNEL-NeuN double-staining showed that apoptosis of hippocampal neurons in APP/PS1 mice was increased compared with that in WT mice, and overexpression of PN-1 reduced apoptosis of hippocampal neurons in APP/PS1 mice (Figure 2(C–D)).