scholarly journals Neuroprotective Effects of OMO within the Hippocampus and Cortex in a D-Galactose and Aβ25–35-Induced Rat Model of Alzheimer’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Shaodong Deng ◽  
Hongmei Lu ◽  
Honggang Chi ◽  
Ying Wang ◽  
Xiao Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Energy Metabolism ◽  
Dose Group ◽  
Control Group ◽  
High Dose ◽  
Antioxidant Enzyme Activities ◽  
Group Model ◽  
Dependent Manner ◽  
Expression Levels

Morinda officinalis F.C. How. (Rubiaceae) is a herbal medicine. It has been recorded that its oligosaccharides have neuroprotective properties. In order to understand the oligosaccharides extracted from Morinda officinalis (OMO), a systematic study was conducted to provide evidence that supports its use in neuroprotective therapies for Alzheimer’s disease (AD). AD rat models were prepared with D-galactose and Aβ25–35. The following groups were used in the present experiment: normal control group, sham-operated group, model group, Aricept group, OMO low-dose group, OMO medium-dose group, and OMO high-dose group. The effects on behavioral tests, antioxidant levels, energy metabolism, neurotransmitter levels, and AD-related proteins were detected with corresponding methodologies. AD rats administered with different doses of OMO all exhibited a significant (P<0.05) decrease in latency and an increase (P<0.05) in the ratio of swimming distance to total distance in a dose-dependent manner in the Morris water maze. There was a significant (P<0.05) increase in antioxidant enzyme activities (SOD, GSH-Px, and CAT), neurotransmitter levels (acetylcholine, γ-GABA, and NE and DA), energy metabolism (Na+/K+-ATPase), and relative synaptophysin (SYP) expression levels in AD rats administered with OMO. Furthermore, there was a significant (P<0.05) decrease in MDA levels and relative expression levels of APP, tau, and caspase-3 in AD rats with OMO. The present research suggests that OMO protects against D-galactose and Aβ25–35-induced neurodegeneration, which may provide a novel strategy for improving AD in clinic.

scholarly journals A novel kit for early diagnosis of Alzheimer’s disease using a fluorescent nanoparticle imaging

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jun Sung Park ◽  
Sang Tae Kim ◽  
Sang Yun Kim ◽  
Min Gi Jo ◽  
Myeong Jun Choi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Diagnosis ◽  
Control Group ◽  
Fluorescent Nanoparticles ◽  
Ht22 Cells ◽  
Expression Levels ◽  
Nanoparticle Imaging ◽  
Fluorescent Nanoparticle ◽  
Primary Focus

Abstract Alzheimer’s disease (AD) is a progressive neurodegenerative disease and chronic illness with long preclinical phases and a long clinical duration. Until recently, a lack of potential therapeutic agents against AD was the primary focus of research, which resulted in less effort directed towards developing useful diagnostic approaches. In this study, we developed a WO2002/088706 kit that is composed of fluorescent nanoparticles for the early detection of AD. We provided a fluorescent nanoparticle for detecting markers and a kit for the early diagnosis of AD. The kit consists of a probe molecule comprising an oligonucleotide capable of detecting one or more AD-specific microRNAs (miRNAs) and biomarkers related to AD. Through screening, we selected miR-106b, miR-146b, miR-181a, miR-200a, miR-34a, miR-124b, miR-153, miR-155, Aβ1-42 monomer (mAβ), Aβ1–42 oligomer (oAβ), UCHL1, NLRP3, Tau, STAT3, SORL1, Clusterin, APOE3, APOE4, Nogo-A, IL-13, and Visfatin to serve as AD- and inflammation-related markers. For detection of kit-binding properties, we checked the expression levels of amyloid beta (Aβ), tau protein, and inflammatory mediators in APP/PS/ApoE knockdown (KD) mice and a control group using co-localisation analysis conducted with a confocal microscope. Using a similar approach, we checked the expression levels of miRNAs in HT22 cells. Finally, we used the plasma from AD patients to confirm that our fluorescent nanoparticles and the WO2002/088706 kit will provide a possible early diagnosis to serve as an AD detector that can be further improved for future studies on targeting AD.

scholarly journals Study on the Effect of Ginsenosides Rb on Blood of Tumor Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Mengmeng Zheng ◽  
Wenxiu Zheng ◽  
Wei Wang ◽  
Hong Guo ◽  
Hui Cao ◽  
...  
Keyword(s):  
Dose Group ◽  
Extraction Process ◽  
Positive Control ◽  
Control Group ◽  
High Dose ◽  
Group Model ◽  
Mice Model ◽  
Distribution Width ◽  
Model Control ◽  
Water Saturated

Objective. The blood of cancer patients is in a state of hypercoagulability, easily leading to thrombosis. Anemia is also a complication of tumors. Anemia and thrombosis affect the treatment of tumor patients. Methods. Ginsenosides Rb were extracted from the stems and leaves of American ginseng using water-saturated ethanol and ethyl acetate in silica gel column. Tumor mice model was established by injecting H22 hepatocellular carcinoma cells into the axilla of mice. Mice were randomly divided into 6 groups: normal control group, model control group, positive control group, low dose group (7 mg/kg), middle dose group (14 mg/kg), and high dose group (35 mg/kg). After 18 days, the blood was obtained by picking the eyeball of mice. The levels of red blood cells (RBC), hemoglobin (HGB), neutrophils/lymphocytes radio (NLR), platelets (PLT), platelet distribution width (PDW), fibrinogen (FIB), and D-Dimer (D-D) were measured and compared in each group of mice. Results. The content of obtained ginsenosides Rb reached 90.05%. This extraction process was simple and reliable. Middle dose of ginsenosides Rb could significantly increase RBC and HGB levels (P<0.05). Moreover, ginsenosides Rb could significantly reduce NLR, PLT, PDW, FIB, and D-D (P<0.01). Conclusion. ginsenosides Rb could significantly improve anaemia and hypercoagulation of blood in cancer mice. Ginsenosides Rb are a potential anticoagulant and antianemia drug in treating cancer.

scholarly journals Promoting Alzheimer's Risk-Reduction through Community-Based Lifestyle Education and Exercise in Rural America: A Pilot Intervention

2020 ◽  
Vol 13 ◽  
pp. 179-185
Author(s):  
Erin Blocker ◽  
Andrew Fry ◽  
Paul Luebbers ◽  
Jeffrey Burns ◽  
Jaime Perales-Puchalt ◽  
...  
Keyword(s):  
Physical Activity ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Reduction ◽  
Healthy Lifestyle ◽  
Control Group ◽  
Dependent Manner ◽  
Community Based ◽  
Supervised Exercise ◽  
Dementia Risk

Introduction. Rural Americans (RA) have poorer vascular health and physical activity levels than their urban counterparts; all are dementia risk factors. Dementia risk reduction among rural individuals requires a tailored approach. The purpose of this project was to examine preliminary efficacy of a community-based physical exercise and/or dementia risk factor-reduction curriculum among rural adults 50 and older. Methods. Seventy-five rural dwelling adults 50 and older were randomized to one of three groups: 1) 10 weeks of Alzheimer’s disease risk-reduction education (ED), 2) risk-reduction education and supervised exercise (EDEX) or 3) control group (CON). Outcomes included baseline to 10-week follow-up difference in dementia knowledge (primary outcome) and physical activity, muscular endurance, healthy lifestyle engagement, and anthropometrics (secondary outcomes). Results. Sixty-nine adults successfully completed the 10-week study. Dementia knowledge increased in a Treatment Arm-dependent manner (χ2 = 6.95 (2), p = 0.03), being ED and EDEX superior to CON. Engagement in healthy lifestyle behaviors did not change statistically. However, participation specifically in physical activity increased over time (χ2 = 11.47 (2), p = 0.003) with EDEX reporting the greatest increases. No significant change in average daily steps was observed for any group. Conclusion. The results suggested dementia risk-reduction education, both with and without structured exercise, leads to improvements in dementia knowledge. When coupled with regular, supervised exercise, this education intervention also helped participants increase engagement in physical activity over 10 weeks. Tailored interventions that combine Alzheimer’s disease education and regular, supervised exercise may help reduce dementia risk in rural communities.

scholarly journals Effects of memantine and high dose vitamin D on gait in the APP/PS1 mouse model of Alzheimer's disease following vitamin D deprivation

2021 ◽  
Author(s):  
Dana N Broberg ◽  
Dickson Wong ◽  
Miranda Bellyou ◽  
Manuel Montero-Odasso ◽  
Olivier Beauchet ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Amyloid Β ◽  
Glutamate Toxicity ◽  
Control Group ◽  
High Dose ◽  
Standard Diet ◽  
Deficient Diet ◽  
Gait Performance

Background: Altered gait is a frequent feature of Alzheimer's disease (AD), as is vitamin D deficiency. Treatment with memantine and vitamin D can protect cortical axons from exposure to amyloid-β and glutamate toxicity, suggesting this combination may mitigate altered gait in AD. Objective: Investigate the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on gait performance in APPswe/PS1dE9 mice. Methods: Male APPswe/PS1dE9 mice were split into four groups (n=14 each) at 2.5 months of age. A control group was fed a standard diet throughout while the other three groups started a vitamin D-deficient diet at month 6. The VitD- group remained on this deficient diet for the rest of the study. At month 9, the remaining two groups began treatment with either memantine alone or memantine combined with 10 IU/g of vitamin D. Gait performance was assessed at months 6, 9, 12, and 15. Results: Vitamin D deprivation led to a 13% increase in hind stride width by month 15 (p<0.001). Examination of the treatment groups at month 15 revealed that mice treated with memantine alone still showed an increase in hind stride width compared to controls (p<0.01), while mice treated with memantine and vitamin D did not (p=0.21). Conclusion: Vitamin D deprivation led to impaired postural control in the APPswe/PS1dE9 model. Treatment with memantine and vitamin D, but not memantine alone, prevented this impairment. Future work should explore the potential for treatments incorporating vitamin D supplementation to improve gait in people with AD.

scholarly journals Neuroprotective Effects of Probiotic-Supplemented Diet on Cognitive Behavior of 3xTg-AD Mice

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
Chenxi Tan ◽  
Yang Liu ◽  
Huiyi Zhang ◽  
Cihan Di ◽  
Dechao Xu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Western Blot ◽  
Water Maze ◽  
Intestinal Flora ◽  
Gene Sequencing ◽  
Learning Ability ◽  
Control Group ◽  
Expression Levels ◽  
Y Maze

Alzheimer’s disease (AD) is recognized as one of the most common types of senile dementia. AD patients first suffer memory loss for recent events (short-term memory impairment). As the disease progresses, they are deprived of self-awareness. This study aims to explore the effects of a probiotic-supplemented diet on the cognitive behaviors and pathological features of mouse models of Alzheimer’s disease (AD). Mice in the control group and the 3xTg-AD group were fed a regular diet and a probiotic-supplemented diet, respectively, for 20 weeks. Behavioral experiments like Morris’s water maze and Y maze were conducted. Then, feces of mice were collected for 16S sRNA gene sequencing for microorganisms. In the end, soluble and insoluble Aβ40 and Aβ42 in the hippocampus and cortex of mice in each group were quantitatively analyzed with a double-antibody Sandwich ELISA. The expression levels of tau protein and gliocyte in the hippocampus and cortex were detected using the Western Blot method. The result of the Morris water maze experiment indicated that, in the place navigation test, the mice in the 3xTg-AD group experienced a significant decline in the learning ability and a longer escape latency and in the space exploration test, the swimming time of mice in the 3xTg-AD group in the target quadrant decreased and after being treated with the probiotic diet, mice in the 3xTg-AD group had improved learning and memory ability. The result of Y maze showed that the probiotic diet can improve the spontaneous alternation accuracy of mice in the 3xTg-AD group. The result of 16s rRNA gene sequencing showed that, compared with mice in the WT group, those in the 3xTg-AD group experienced a change in the intestinal flora. The Western Blot result displayed a decreased expression level of tau (pS202) ( P < 0.05 ) and decreased expression levels of Iba-1 and GFAP ( P < 0.05 ). The result of the ELISA experiment showed decreased levels of soluble and insoluble Aβ40 and Aβ42 in 3xTg-AD mice ( P < 0.05 ). In conclusion, a probiotic diet can prevent and treat AD by improving the intestinal flora of 3xTg-AD.

Effects of Memantine and High Dose Vitamin D on Gait in Male APP/PS1 Alzheimer’s Disease Mice Following Vitamin D Deprivation

2021 ◽  
pp. 1-12
Author(s):  
Dana Broberg ◽  
Dickson Wong ◽  
Miranda Bellyou ◽  
Manuel Montero-Odasso ◽  
Olivier Beauchet ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Amyloid Β ◽  
The Other ◽  
Glutamate Toxicity ◽  
Control Group ◽  
High Dose ◽  
Standard Diet ◽  
Deficient Diet

Background: Altered gait is a frequent feature of Alzheimer’s disease (AD), as is vitamin D deficiency. Treatment with memantine and vitamin D can protect cortical axons from exposure to amyloid-β and glutamate toxicity, suggesting this combination may mitigate altered gait in AD. Objective: Investigate the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on gait performance in APPswe/PS1dE9 mice. Methods: Male APPswe/PS1dE9 mice were split into four groups (n = 14 each) at 2.5 months of age. A control group was fed a standard diet throughout while the other three groups started a vitamin D-deficient diet at month 6. One group remained on this deficient diet for the rest of the study. At month 9, the other two groups began treatment with either memantine alone or memantine combined with 10 IU/g of vitamin D. Gait was assessed using CatWalk at months 6, 9, 12, and 15. Results: Vitamin D deprivation led to a 13% increase in hind stride width by month 15 (p <  0.001). Examination of the treatment groups at month 15 revealed that mice treated with memantine alone still showed an increase in hind stride width compared to controls (p <  0.01), while mice treated with memantine and vitamin D did not (p = 0.21). Conclusion: Vitamin D deprivation led to impaired postural control in the APPswe/PS1dE9 model. Treatment with memantine and vitamin D, but not memantine alone, prevented this impairment. Future work should explore the potential for treatments incorporating vitamin D supplementation to improve gait in people with AD.

scholarly journals Influence of nonylphenol exposure on basic growth, development, and thyroid tissue structure in F1 male rats

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7039
Author(s):  
Lin Wang ◽  
Jie Xu ◽  
Feng Zeng ◽  
Xiangjun Fu ◽  
Weihong Xu ◽  
...  
Keyword(s):  
Dose Group ◽  
Corn Oil ◽  
Thyroid Tissue ◽  
Male Rats ◽  
Follicular Epithelium ◽  
High Dose Group ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Lactational Exposure

Objective Environmental endocrine disruptors (EEDs) with a weak ability to mimic estrogen have been associated with thyroid dysfunction. However, little is known about the effect of nonylphenol (NP), a well-known EED, on thyroid structure. The present study evaluates whether gestational and lactational exposure to NP impacts growth and thyroid structure in F1 male rats. Methods A total of 60 rats were gavaged with NP (25, 50, and 100 mg/kg), estradiol (E2, 30 μg/kg/day), and corn oil alone (vehicle control) from gestational day 6 to postnatal day (PND) 21. Serum thyroid hormones free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone levels were detected by automated chemiluminescence immunoassay analyzer. The NP level in the thyroid was measured using high-performance liquid chromatography. The ultrastructure of follicular epithelial cells was examined using transmission electron microscopy. Histopathology was conducted using hematoxylin and eosin staining. Results On PND 0, exposure to 50 and 100 mg/kg/day NP led to a significant decrease in the average litter size, litter weight and number of live pups per litter compared to the control group (P < 0.05). Dams exposed to NP during perinatal period demonstrated decreased serum levels of FT3 and FT4 in F1 male rats, when compared to the control group (P < 0.05). The NP level in the control group was 3.39 ± 0.08 ng/mg, while NP levels in the low, middle, and high dose groups ranged from 5.20 to 11.00 ng/mg. Exposure caused a dose-related increase in NP level in the thyroid of male pups (P < 0.01). The thicknesses of the thyroid follicular epithelium were 2.06 ± 0.37 μm in the control group and 3.97 ± 1.61 μm in the high-dose group. The thickness of the thyroid follicular epithelium increased with an increase in treatment dose in a dose-dependent manner (P < 0.05). The sizes of the thyroid follicles were 1,405.53 ± 866.62 μm2 in the control group and 317.49 ± 231.15 μm2 in the high-dose group. With increasing NP dosages, animals showed a decreased size of the thyroid follicle (P < 0.01). Thyroid follicular cells of NP-treated rats showed mildly swollen mitochondria and dilated rough endoplasmic reticulum in the cytoplasm. Conclusion Nonylphenol can cross the placental barrier and accumulate in the thyroid of F1 male rats. Gestational and lactational exposure to NP in dams impacted both development and growth of pups and damaged the ultrastructure of their thyroid tissue, which may further negatively influence normal thyroid function.

scholarly journals Effects of Phenylethanoid Glycosides Extracted from Herba Cistanches on the Learning and Memory of the APP/PSI Transgenic Mice with Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jianhua Yang ◽  
Bowei Ju ◽  
Junping Hu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Group Model ◽  
Model Group ◽  
Active Components ◽  
Phenylethanoid Glycosides ◽  
Step Down

Background. To investigate the effects of phenylethanoid glycosides (PhGs) extracted from Herba Cistanches on the behavioral and cognition capacity of the APP/PSI transgenic mice with Alzheimer’s disease (AD). Methods. AD mice were randomly divided into the control group, model group, donepezil group, PhG groups, and verbascose group, respectively. Three weeks later, the animals were subject to behavioral and cognition evaluation by the nesting test, Morris water maze test, and step-down test. Results. The cognition capacity in these groups showed a significant increase compared with that in the model group. The step-down test indicated that the errors induced by the memory decrease in the PhG groups and verbascose group showed a significant decrease compared with those in the model group ( P < 0.05 ). Conclusions. PhGs attenuated the cognitive dysfunction features of the APP/PSI transgenic gene. Besides, PhGs were the active components for the anti-AD activity of H. Cistanches.

scholarly journals Effects of DI-(2-Ethylhexyl) Phthalate on Rat Ovarian Function

2011 ◽  
Vol 30 (4) ◽  
pp. 309-316
Author(s):  
Cheng-kang Xu ◽  
Xiao-hong Wang ◽  
Shuang-bo Tang
Keyword(s):  
Estrous Cycle ◽  
Dose Group ◽  
Low Dose ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Short Course ◽  
Long Course ◽  
Ethylhexyl Phthalate ◽  
Medium Dose

Effects of DI-(2-Ethylhexyl) Phthalate on Rat Ovarian FunctionThis study aimed to evaluate the effects of di-(2-ethylhexyl)phthalate (DEHP) on estrous cycle, sex hormone levels and ovary histological features. A total of 80 female SD rats were randomly divided into 8 groups (n=10 per group): short-course control group, short-course low-dose group, short-course medium-dose group, and short-course high-dose group, long-course control group, long-course low-dose group, long-course medium-dose group and long-course high-dose group. Intragastrical DEHP was administrated at 1000 mg/kg/d (low dose), 2000 mg/kg/d (medium dose) and 3000 mg/kg/d (high dose) independently for 14 days (short course) or 28 days (long course). Rats in control groups were untreated. Vaginal smearing was used to detect the estrous cycle and rats were weighed at every Monday and Thursday to evaluate the growth status. At the end of study, rats were sacrificed and bilateral ovaries were obtained for histological examination. In addition, ELISA determined levels of serum progesterone, estradiol, testosterone, follicle stimulating hormone and luteinizing hormone. DEHP treatment limited body weight gain (p<0.05), prolonged the estrous cycle (p<0.05), decreased the ovarian mass index (p<0.05) and ovarian weight. No evident degeneration, necrosis or other pathological features were found in the ovaries. The testosterone levels were decreased by DEHP treatment in a dose dependent manner. DEHP treatment could increase serum testosterone level, inhibit ovulation and prolong the estrous cycle of rats, exerting reproductive toxicity in a dose dependent manner. We speculate DEHP can affect the endocrine regulatory function of the ovary and limit the body weight gain, resulting in chronic toxicity.

scholarly journals Unearthing of Key Genes Driving the Pathogenesis of Alzheimer’s Disease via Bioinformatics

2021 ◽  
Vol 12 ◽  
Author(s):  
Xingxing Zhao ◽  
Hongmei Yao ◽  
Xinyi Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Temporal Cortex ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Machine Learning Algorithms ◽  
Functional Enrichment ◽  
Control Group ◽  
Hub Genes ◽  
Expression Levels

Alzheimer’s disease (AD) is a neurodegenerative disease with unelucidated molecular pathogenesis. Herein, we aimed to identify potential hub genes governing the pathogenesis of AD. The AD datasets of GSE118553 and GSE131617 were collected from the NCBI GEO database. The weighted gene coexpression network analysis (WGCNA), differential gene expression analysis, and functional enrichment analysis were performed to reveal the hub genes and verify their role in AD. Hub genes were validated by machine learning algorithms. We identified modules and their corresponding hub genes from the temporal cortex (TC), frontal cortex (FC), entorhinal cortex (EC), and cerebellum (CE). We obtained 33, 42, 42, and 41 hub genes in modules associated with AD in TC, FC, EC, and CE tissues, respectively. Significant differences were recorded in the expression levels of hub genes between AD and the control group in the TC and EC tissues (P &lt; 0.05). The differences in the expressions of FCGRT, SLC1A3, PTN, PTPRZ1, and PON2 in the FC and CE tissues among the AD and control groups were significant (P &lt; 0.05). The expression levels of PLXNB1, GRAMD3, and GJA1 were statistically significant between the Braak NFT stages of AD. Overall, our study uncovered genes that may be involved in AD pathogenesis and revealed their potential for the development of AD biomarkers and appropriate AD therapeutics targets.

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