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 Nrf2 Ablation Promotes Alzheimer’s Disease-Like Pathology in APP/PS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Peng Ren ◽  
Jingwei Chen ◽  
Bingxuan Li ◽  
Mengzhou Zhang ◽  
Bei Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
Related Factor ◽  
Qrt Pcr

Introduction. Alzheimer’s disease (AD), the most common neurodegenerative disorder, is characterized by the accumulation of amyloid-β (Aβ) peptide and hyperphosphorylated tau protein. Accumulating evidence has revealed that the slow progressive deterioration of AD is associated with oxidative stress and chronic inflammation in the brain. Nuclear factor erythroid 2- (NF-E2-) related factor 2 (Nrf2), which acts through the Nrf2/ARE pathway, is a key regulator of the antioxidant and anti-inflammatory response. Although recent data show a link between Nrf2 and AD-related cognitive decline, the mechanism is still unknown. Thus, we explored how Nrf2 protects brain cells against the oxidative stress and inflammation of AD in a mouse model of AD (APP/PS1 transgenic (AT) mice) with genetic removal of Nrf2. Methods. The spatial learning and memory abilities of 12-month-old transgenic mice were evaluated using a Morris water maze test. Hippocampal levels of Nrf2, Aβ, and p-tauS404 and of astrocytes and microglia were determined by immunostaining. Inflammatory cytokines were determined by ELISA and quantitative real-time polymerase chain reaction (qRT-PCR). Oxidative stress was measured by 8-hydroxydeoxyguanosine immunohistochemistry, and the antioxidant response was determined by qRT-PCR. Results. The spatial learning and memory abilities of AT mice were impaired after Nrf2 deletion. Aβ and p-tauS404 accumulation was increased in the hippocampus of AT/Nrf2-KO mice. Astroglial and microglial activation was exacerbated, followed by upregulation of the proinflammatory cytokines IL-1β, IL-6, and TNF-α. Conclusion. Our present results show that Nrf2 deficiency aggravates AD-like pathology in AT mice. This phenotype was associated with increased levels of oxidative and proinflammatory markers, which suggests that the Nrf2 pathway may be a promising therapeutic target for AD.

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 Ultrasound Mediated Microbubbles Destruction Assists Dual Delivery of Beta-amyloid Antibody and NSCs to Restore Neural Function in Transgenic Mice of Alzheimer’s Disease

2020 ◽  
Author(s):  
qiong Zhu ◽  
hai Cui ◽  
yiyi Liao ◽  
xue Guan ◽  
ying He ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Targeted Delivery ◽  
Function Evaluation ◽  
Control Group ◽  
Neural Function ◽  
Imaging Method ◽  
The Us ◽  
Β Amyloid

Abstract Background : To explore the feasibility, efficacy and safety of ultrasound mediated microbubbles destruction（UMMD） assisted dual delivery of β-amyloid antibody loaded by microbubbles (MB Aβ ) and neural stem cells (NSCs) on Alzheimer’s disease（AD）. Methods : 27 APP/PS1 double transgenic mice and 33 wild-type mice were used. The dual delivery of β-amyloid antibody and NSCs group (US+MB Aβ +NSCs), single delivery of β-amyloid antibody group (US+MB Aβ ), US+MB group, Control group and Wild group, were involved in the experiment. MB Aβ or MB were injected via the tail vein, followed by NSCs or saline administration and exposed to ultrasound once a week for four times. The survival of NSCs was detected with the in vivo imaging method. Mice in each group were used for behavioral function evaluation and the pathology tests. Brain samples were used to detect β-amyloid deposition, BDNF and synaptophysin expression. Results : BBB was opened by UMMD with an opening time about 10 h. The transplanted NSCs survived in AD brain for no more than 72 h. The learning and spatial memory function was significantly improved in the US+MB Aβ +NSCs group, US+MB Aβ group came second. Immunochemistry results showed amyloid plaques reduction in the US+MB Aβ +NSCs group at the cortex and hippocampus. Higher level of BDNF was demonstrated in the US+MB Aβ +NSCs group than the US+MB Aβ group and the Control group with Western Blot and immunofluorescence examination, but synaptophysin remained no significant changes. Conclusions : UMMD assisted combined delivery of β-amyloid antibody and NSCs to AD mice brain can help to clear the Aβ peptide, increase BDNF level and restore the impaired neural function, which was superior to β-amyloid antibody delivery group. Therefore, the combined targeted delivery assisted by UMMD strategy may be a promising and safe method on treating AD.

scholarly journals Effect of Piper betel leaf extract on learning and memory in Aluminium chloride induced Alzheimer’s disease in Wistar rats

2019 ◽  
Vol 12 (3) ◽  
pp. 1425-1431
Author(s):  
Shreeraksha Upadhyaya ◽  
Shivaprakash Gangachannaiah ◽  
Pallavi Lakshmi Chandrashekar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Wistar Rats ◽  
Treated Group ◽  
Aluminium Chloride ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Betel Leaf ◽  
Maze Test ◽  
Piper Betel Leaf

Alzheimer's disease is a common neurological disorder affecting a significant proportion of the elderly population.There are only a few drugs which can be used safely to treat it. We sought to investigate for the first time Piper betel leaf, a postmeal mouth freshener for its potential use in Alzheimer's disease. Five groups of male Wistar rats with six rats in each group aged 10-12 weeks were used. The control group received the distilled water, aluminium chloride (AlCl3) group was treated with AlCl3, the standard group was treated with rivastigmine with AlCl3, and the two test groups received piper betel leaf extract (PBE) at doses of 400mg/kg and 500mg/kg body weight with AlCl3. AlCl3 was administered orally for 42 days in all the treated groups. Memory and learning were evaluated by Morris water maze test and Passive avoidance test.The results of the Morris water maze test showed reduced mean escape latency period in all the groups on trial day three (P≤0.05) and on trial day four (P ≤0.01) compared to AlCl3 group. The retention of spatial memory by probe trial showed that PBE and rivastigmine treated group spent more time in the target (platform) quadrant when compared to AlCl3 group (P≤0.01). The passive avoidance test showed a significant increase in step through latency in standard and test groups compared to the AlCl3 treated group. The weight of the rats treated with AlCl3 and PBE was reduced at the end of the treatment period while increased in standard and control group. The study shows the beneficial effects of Piper betel leaves in Alzheimer’s disease by significantly improving the learning and memory functions in rats.

scholarly journals A UPLC-Q-TOF/MS-Based Metabolomics Study on the Effect of Corallodiscus flabellatus (Craib) B. L. Burtt Extract on Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yang-Yang Wang ◽  
Ning Zhou ◽  
Yan-Po Si ◽  
Zhi-Yao Bai ◽  
Meng Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Metabolite Profiling ◽  
Huperzine A ◽  
Control Group ◽  
Model Group ◽  
Metabolomics Study ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse ◽  
Tof Ms

A UPLC-Q-TOF/MS-based metabolomics study was carried out to explore the intervening mechanism of Corallodiscus flabellatus (Craib) B. L. Burtt (CF) extract on Alzheimer’s disease (AD). The AD model group consisted of senescence-accelerated mouse prone 8 (SAMP8) mice, and the control group consisted of senescence-accelerated mouse resistant 1 (SAMR1) mice. UPLC-Q-TOF/MS detection, multivariate statistical analysis, and pathway enrichment were jointly performed to research the change in metabolite profiling in the urine of AD mice. The result suggested that the metabolite profiling of SAMP8 mice significantly changed at the sixth month compared with SAMR1 mice of the same age, and the principal component analysis (PCA) score scatter plots of the CF group closely resembled those of the control and positive drug (huperzine A, HA) group. A total of 28 metabolites were considered potential biomarkers associated with the metabolism of beta-alanine, glycine, serine, threonine, cysteine, methionine, arginine, proline, and purines in AD mice. Furthermore, the CF group was clustered with the control and positive group and was clearly separated from the model group in the heat map. In conclusion, significant anti-AD effects were firstly observed in mice after treatment with the CF extract, and the urinary metabolomics approach assisted with dissecting the underlying mechanism.

scholarly journals Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer’s Disease Model Rats by Maintaining Synaptic Plasticity

2018 ◽  
Vol 17 (5) ◽  
pp. 389-399 ◽  
Author(s):  
Kai Wang ◽  
Weiming Sun ◽  
Linlin Zhang ◽  
Wei Guo ◽  
Jiachun Xu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Oleanolic Acid ◽  
Memory Deficit ◽  
Sham Operation ◽  
Group Model ◽  
Model Group ◽  
Sham Operation Group ◽  
Operation Group

Background: Abnormal amyloid β (Aβ) accumulation and deposition in the hippocampus is an essential process in Alzheimer’s disease (AD). Objective: To investigate whether Oleanolic acid (OA) could improve memory deficit in AD model and its possible mechanism. Methods: Forty-five SD rats were randomly divided into sham operation group, model group, and OA group. AD models by injection of Aβ25-35 were built. Morris water maze (MWM) was applied to investigate learning and memory, transmission electron microscope (TEM) to observe the ultrastructure of synapse, western blot to the proteins, electrophysiology for long-term potentiation (LTP), and Ca2+ concentration in synapse was also measured. Results: The latency time in model group was significantly longer than that in sham operation group (P=0.0001); while it was significantly shorter in the OA group than that in model group (P=0.0001); compared with model group, the times of cross-platform in OA group significantly increased (P=0.0001). TEM results showed OA could alleviate neuron damage and synapses changes induced by Aβ25-35. The expressions of CaMKII, PKC, NMDAR2B, BDNF, TrkB, and CREB protein were significantly improved by OA (P=0.0001, 0.036, 0.041, 0.0001, 0.0001, 0.026, respectively) compared with that in model group; the concentration of Ca2+ was significantly lower in OA group (1.11±0.42) than that in model group (1.68±0.18); and the slope rate (P=0.0001) and amplitude (P=0.0001) of f- EPSP significantly increased in OA group. Conclusion: The present results support that OA could ameliorate Aβ-induced memory loss of AD rats by maintaining synaptic plasticity of the hippocampus.

scholarly journals Effect of Donepezil and Hyoscyamoside on Improving Spatial Memory in Rats With Alzheimer's Disease

2020 ◽  
Vol 23 (4) ◽  
pp. 524-539
Author(s):  
Fatemeh Heidari Soureshjani ◽  
◽  
Majid Kheirollahi ◽  
Parichehreh Yaghmaei ◽  
Fattah Sotoodehnejadnematalahi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Beta Amyloid ◽  
Male Rats ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Treatment Groups

Background and Aim: Alzheimerchr('39')s Disease (AD) is a neurodegenerative brain disease that gradually destroys memory and cognitive skills. The disease is caused by the formation of beta-amyloid plaques, oxidative stress, dysfunctions in the cholinergic system, neuronal killing inflammation, and ultimately brain atrophy. Donepezil and hyoscyamoside have inhibitory effects on these pathogens; therefore, their impact on the learning process of Alzheimer’s rats in the Morris Water Maze was investigated. Methods & Materials: In the present experimental study, 60 male rats of Wistar breed with approximately 7 weeks age within the control group (rats that received normal water and food), the PBS group (underwent surgery), PBS group (received solvent Aβ), the first Alzheimer›s group (animals that received beta-amyloid by Alzheimer’s surgery, second Alzheimer’s group (after Alzheimer’s surgery, they received 1 cc of normal saline daily, and treatment groups that treated the rats with beta-amyloid after Alzheimer. In the hyoscyamoside group, they received 10 mg/kg daily of hyoscyamoside for 28 days. The donepezil group received it 4 mg/kg daily for 28 days by gavage. The Morris Water Maze test was used to evaluate learning and memory. Data were analyzed by ANOVA statistical analysis and Post Hoc test. Ethical Considerations: The Ethics Committee in Biomedical Research, Islamic Azad University, Science and Research Branch approved the research (Code: IR.IAU.SRB.REC 1397.057) Results: Beta-amyloid injection caused extensive damage to memory. The treatment groups with hyoscyamoside and donepezil spent less time and distance with a significant level (P<0.001) than the group of Alzheimer’s patients to find the hidden platform. In the reminder phase, where the previously hidden platform was located, they spent more time, with a significant level (P<0.001) in the local quarter. Conclusion: Treatment of rats with hyoscyamoside and donepezil improved spatial memory in Alzheimer’s rats. They appear to play a significant role in the prevention and treatment of Alzheimer’s disease.

scholarly journals Effects of manual acupuncture combined with donepezil in a mouse model of Alzheimer’s disease

2019 ◽  
Vol 37 (1) ◽  
pp. 64-71
Author(s):  
Jing Jiang ◽  
Gang Liu ◽  
Suhua Shi ◽  
Yujie Li ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Combined Therapy ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Manual Acupuncture ◽  
Male Mice ◽  
Model Of Alzheimer’S Disease ◽  
Aβ Amyloid

Objectives: To explore whether combined therapy with donepezil and acupuncture is better than treatment with donepezil or acupuncture individually in a rat model of Alzheimer’s disease. Methods: In this study, we randomly divided 40 7.5-month-old senescence-accelerated mouse prone 8 (SAMP8) male mice into four groups: SAMP8, SAMP8+D, SAMP8+MA and SAMP8+D+MA. An additional 10 7.5-month-old SAMR1 male mice were included as a healthy control group (SAMR1). Mice in the SAMP8+D group were given donepezil at a dose of 0.65 µg/g/day; mice in the SAMP8+MA group underwent manual acupuncture at GV20, GV26 and Yintang for 20 min per day; mice in the SAMP8+D+MA received both donepezil and manual acupuncture; and mice in the SAMR1 and SAMP8 groups underwent restraint only to control for the effects of handling. After the 15-day treatment, the Morris water maze test, micro-PET(positron-emission tomography), H&E (haematoxylin and eosin) staining, and immunohistochemistry were used to study the differences between donepezil (SAMP8+D), acupuncture (SAMP8+MA), and donepezil combined with acupuncture (SAMP8+D+MA) therapy for the treatment of Alzheimer’s disease. Results: We found that, compared with the untreated SAMP8 group, donepezil, manual acupuncture, and combined therapy with donepezil and manual acupuncture all improved spatial learning and memory ability, the level of glucose metabolism in the brain, and the content of Aβ amyloid in the cortex. Moreover, combined therapy outperformed treatment with donepezil or acupuncture individually in the SAMP8 mice. Conclusion: This study shows that the combination of manual acupuncture and donepezil in an Alzheimer’s disease animal model is superior to acupuncture and donezepil alone. However, randomised controlled trials should be undertaken to clarify the clinical efficacy of combination therapy.

scholarly journals NLRC3 delays the progression of AD in APP/PS1 mice via inhibiting PI3K activation

2019 ◽  
Author(s):  
lihuang zha ◽  
Zai-xin Yu ◽  
Shuhong Guo ◽  
Li Zhou ◽  
Wen Guo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Inflammatory Responses ◽  
Behavioral Experiment ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Hippocampus Slice ◽  
Pi3k Activation ◽  
Brain Tissues

Abstract Background/Aims: NLRC3 inhibits inflammatory responses. Epidemiological studies indicate that neuroinflammation induces and accelerates the onset of Alzheimer's disease (AD). This study was designed to determine whether NLRC3 plays a role in neuroinflammation, Aβ accumulation and neuroprotection in AD mice. Methods: Thirty 12-month-old APP/PS1 transgenic mice were randomized into three groups as model group, APP/PS1 +LVCON307 and APP/PS1 +LV-NLRC3 group. Ten 12-month-old wild-type C57 mice were chosen as control group. Mice in APP/PS1 +LVCON307 and APP/PS1 +LV-NLRC3 group were injected with LVCON307 or LV-NLRC3 through intracerebroventricular injection. Six months after LVCON307 or LV-NLRC3 injection, We carried out Morris water maze test on mice and harvested their brain tissues after the behavioral experiment. The deposition of amyloid protein and the changes of Nissle bodies were observed by ThS and Nissle staining. The expressions of NLRC3, 6E10, GFAP, Iba1, NeuN and PI3K were detected by immunohistochemistry or immunofluorescence. Western blot was used to analyze the expression of NLRC3, PI3K, GFAP and Iba1. Results: The expression of NLRC3 is down-regulated in brain tissues of APP/PS1 mice. Mice in APP/PS1 group had a significant attenuation of learning and memory ability compared to the control group, the ability of learning and memory was improved in APP/PS1 +LV-NLRC3 mice. The expression of 6E10, GFAP, Iba1 and PI3K in brain and hippocampus slice of APP/PS1 and APP/PS1 + LVCON307 mice were significantly higher than those of the control group, while the expression of NLRC3 and NeuN was significantly lower than that of the control group. After overexpression of NLRC3, the expression of 6e10, GFAP, Iba1 and PI3K in APP/PS1 + LV-NLRC3 group was significantly lower than that in APP/PS1 and APP/PS1 + LVCON307 group, while the expression of NLRC3 and NeuN was significantly higher than that in APP/PS1 and APP/PS1 + LVCON307 group. NLRC3 co-localized with NeuN. PI3K activation with 740YP increased the expression of GFAP and Iba-1 in hippocampus with exogenous NLRC3 protein. Conclusion: NLRC3 may play an important role in the development and progression of AD. Down-regulation of NLRC3 can lead to the activation of PI3K, resulting in abnormal plaque deposition, glial cell activation and neuron loss during AD. NLRC3 delays the progression of AD in APP/PS1 mice via inhibiting PI3K activation. Keywords: NLRC3 • inflammation • Aβ • neuron •PI3K •Alzheimer's disease

Electroacupuncture Improves Cognitive Deficits and Activates Ppar-γ in a Rat Model of Alzheimer's Disease

2017 ◽  
Vol 35 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Min Zhang ◽  
Gui-Hua Xv ◽  
Wei-Xin Wang ◽  
Di-Juan Meng ◽  
Yan Ji
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Rat Model ◽  
Morris Water Maze Test ◽  
Model Group ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Ppar Γ ◽  
Hippocampal Ca1

Background Alzheimer's disease (AD) is an age-associated neurodegenerative disorder that is associated with a progressive impairment of cognition. Acupuncture has protective effects, although the molecular mechanisms are largely unknown. The activation of peroxisome proliferator activated receptor γ (PPAR-γ) has an impact on the pathogenesis of AD. Objective To test the hypothesis that electroacupuncture (EA) confers therapeutic benefits through activation of PPAR-γ in a rat model of AD. Methods 80 male Sprague-Dawley rats were randomly divided into four groups (n=20 each): Control (healthy control group), Sham (sham-operated group), AD (untreated AD model group), and AD+EA (AD model group treated with EA). The AD model was induced in the latter two groups by injection of amyloid-β (Aβ)1-40 into the hippocampal CA1 area bilaterally. EA was administered at GV20 and BL23 six times per week for 4 weeks. The rats’ behaviour was examined using the Morris water maze test, and protein expression of Aβ, hyperphosphorylated tau protein (p-Tau), PPAR-γ, and hyperphosphorylated p38 mitogen activated protein kinase (p38MAPK) in the hippocampal CA1 region was examined by immunohistochemistry and Western blotting. Results EA significantly improved cognitive deficits and reduced Aβ and p-Tau Ser404 protein concentrations in the hippocampal CA1 region. AD decreased PPAR-γ and increased p-p38MAPK, while EA significantly upregulated PPAR-γ expression and significantly downregulated p-p38MAPK expression. Conclusions Acupuncture at GV20 and BL23 might have a beneficial effect on rats with AD via activation of PPAR-γ and inhibition of p-p38MAPK expression.

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