scholarly journals Memory Enhancing Activity of Saraswatarishta in Mice

2020 ◽  
Vol 13 (4) ◽  
pp. 2033-2039
Author(s):  
Bhagyashri D. Rajopadhye ◽  
Ranjana A. Sahasrabudhe
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Disease Incidence ◽  
Preventive Measure ◽  
Current Treatment ◽  
Control Group ◽  
Group I ◽  
Memory Enhancing

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a gradual decline in memory. Incidence of Alzheimer's disease increases with age. The disease incidence is 1% in 60 year olds & increases to 30 % at 85 years age. Hence this disease is already having enormous magnitude in today's graying world. Current treatment of Alzheimer’s disease includes- cholinesterase inhibitors& N-methyl- D-aspartate antagonists, but the benefit observed is modest. In traditional medicine Saraswatarishta is being used as memory enhancer for centuries. Brahmi, one of its major ingredients, is also being used to treat Alzheimer’s. So present study was undertaken for authentication of traditional claims of Saraswatarishta as a memory-enhancing agent. Five groups of mice (6 mice in each) were used for this study. Control group (group I) received distilled water, Group II received Saraswatarishta (2.5ml/kg) single dose and Group III received Saraswatarishta (2.5ml/kg) for 2wks. Group IV was given Diazepam (1mg/kg) to produce amnesia. For Group V, Saraswatarishta (2.5ml/kg) was given for 2wks followed by Diazepam (1mg/kg). Effect of Saraswatarishta on learning and memory of mice was studied using elevated plus maze model (EPM). Reduction in TL (Transfer Latency) indicates improvement in learning or memory and prolongation indicates impairment. Diazepam induced prolongation of TL is an accepted model of dementia. In our study, 2 weeks daily treatment of Saraswatarishta completely prevented impairment of learning and memory by Diazepam, corroborating the Ayurvdic use of Saraswatarishta and Brahmi, its major ingredient in the management of dementia. Saraswatarishta can be used as preventive measure to overcome demensia in Alzheimer’s disease.

scholarly journals Experimental and Computational Studies to Characterize and Evaluate the Therapeutic Effect of Albizia lebbeck (L.) Seeds in Alzheimer’s Disease

Medicina ◽  
2019 ◽  
Vol 55 (5) ◽  
pp. 184 ◽  
Author(s):  
Uzma Saleem ◽  
Zohaib Raza ◽  
Fareeha Anwar ◽  
Bashir Ahmad ◽  
Sundas Hira ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Neurodegenerative Disorder ◽  
Control Group ◽  
Albino Rats ◽  
Computational Studies ◽  
Behavioral Tests ◽  
Albizia Lebbeck ◽  
Group I

Background and Objectives: Alzheimer’s disease (AD) is a neurodegenerative disorder that deteriorates daily life due to loss of memory and cognitive impairment. It is believed that oxidative stress and cholinergic deficit are the leading causes of AD. Disease-modifying therapies for the treatment of AD are a challenging task for this century. The search for natural and synthetic agents has attracted the attention of researchers. The objective of this study was a scientific approach to search for most suitable remedy for AD by exploiting the potential of Albizia lebbeck (L.) seeds. Materials and Methods: Hydromethanolic extract of Albizia lebbeck seeds (ALE) was prepared by maceration. The plant was characterized by physico-chemical, phyto-chemical, and high-performance liquid chromatography (HPLC). Thirty-six Wistar albino rats were used in this study and divided into six groups (n = 6). Group I: normal control; Group II: disease control (AlCl3; 100 mg/kg); Group III: standard control (galantamine; 0.5 mg/kg); Groups IV–VI were treated ALE at 100, 200 and 300 mg/kg dose levels, respectively. All the treatments were given orally for 21 consecutive days. Y-maze, T-maze, Morris water maze, hole board, and open field behavioral tests were performed to analyze the cognitive impairment. Biochemical, histological, and computational studies were performed to support the results of behavioral tests. Results: HPLC analysis indicated the presence of quercetin, gallic acid, m-coumaric acid, and sinapic acid. ALE significantly improved the memory and cognitive impairments. Endogenous antioxidant stress biomarker levels and histopathological outcomes supported the therapeutic potential of A. lebbeck in AD. Cholinergic deficits were also ameliorated by ALE co-administration, possibly by the inhibition of hyperactive acetylcholinesterase (AChE). Docking studies supported the potential of ALE against AD. Conclusions: The data suggested that ALE has neuroprotective potential that can be exploited for beneficial effects to treat AD.

scholarly journals Protective effect of Picrorhiza kurroa on Alzheimer’s disease induced by aluminium chloride in rats

2017 ◽  
Vol 6 (3) ◽  
pp. 602 ◽  
Author(s):  
Somasekhar K. Reddy ◽  
Sudheer A. ◽  
Arunamma M. ◽  
Likitha Sree P. ◽  
Jyothirmayi E.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Aluminum Chloride ◽  
Neurodegenerative Disorder ◽  
Ethanolic Extract ◽  
Aluminium Chloride ◽  
Control Group ◽  
Picrorhiza Kurroa ◽  
Group I ◽  
Brain Acetylcholinesterase

Background: Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive deterioration together with declining activities of daily living and behavioural changes. The present work is aimed to investigate the effect of methanolic extract of rhizomes of Picrorhiza kurroa against aluminum chloride induced Alzheimer’s disease.Methods: Wistar rats were selected in this study and were divided into 5 groups (6 each). Group I served as normal control. Group II received aluminum chloride (300mg/kg, P.O.). Group III and IV received ethanolic extract of Picrorhiza kurroa (200mg/kg, 400mg/kg, P.O. respectively) and inducing agent (AlCl3 300mg/kg, P.O.). Group V received rivastigmine (0.3mg/kg, I.P.) and inducing agent (AlCl3 300mg/kg, P.O.). The rats were given respective treatment for 20 days and behavioural parameters were determined on 20th day. After 20th day rats were sacrificed and anti-oxidant parameters, brain acetylcholinesterase content were determined.Results: Oral administration of ethanolic extract of Picrorhiza kurroa at doses 200, 400mg/kg body weight showed improve in behavioural parameters when compared to AlCl3 induced rats, showed increase in superoxide dismutase, catalase, reduced glutathione and decreased levels of malondialdehyde and showed decrease in brain acetylcholinesterase content when compared to AlCl3 induced rats.Conclusions: The study clearly demonstrated the beneficial effects of Picrorhiza kurroa by improving biochemical and behavioural parameters.

scholarly journals β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer’s Disease

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 441 ◽  
Author(s):  
Sundas Hira ◽  
Uzma Saleem ◽  
Fareeha Anwar ◽  
Muhammad Farhan Sohail ◽  
Zohaib Raza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Silico ◽  
Control Group ◽  
Enhancement Effect ◽  
Amyloid Β Protein ◽  
Group I ◽  
In Silico Studies ◽  
Β Carotene

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

scholarly journals Effects of Swimming Training and Royal Jelly on BDNF and NGF Gene Expression in Hippocampus Tissue of Rats with Alzheimer’s Disease

2020 ◽  
Vol 22 (2) ◽  
Author(s):  
Amin Dehbozorgi ◽  
Laleh Behbudi Tabrizi ◽  
Seyed Ali Hosseini ◽  
Masod Haj Rasoli
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Royal Jelly ◽  
Neurodegenerative Disorder ◽  
Control Group ◽  
Swimming Training ◽  
Age Related ◽  
And Training ◽  
Ngf Gene

Background: Alzheimer’s disease (AD) is an age-related neurodegenerative disorder. Evidence from neuropathological studies indicates that the levels of neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are compromised in AD. Objectives: The present study aimed to review the effects of swimming training and royal jelly (RJ) on BDNF and NGF gene expression in the hippocampus tissue of rats with AD. Methods: In the present experimental study, 25 rats with AD were divided into five groups, including (1) control, (2) sham, (3) RJ, (4) training, and (5) training with RJ. Five healthy rats were selected as the healthy control group to examine the effect of AD induction by 8 mg/kg trimethyltin chloride (TMT) intra-peritoneally on BDNF and NGF. During eight weeks, groups 3 and 5 received 100 mg/kg RJ daily intra-peritoneally, and groups 4 and 5 swam in a rat swimming tank three sessions per week. One-way ANOVA with Tukey’s post hoc test was used for data analysis in SPSS 20 software (P < 0.05). Results: The induction of AD by TMT had a significant effect on the reduction of BDNF (P = 0.001) and NGF (P = 0.001). However, RJ had a significant effect on the increase of NGF (P = 0.03). Nevertheless, RJ (P = 0.99), training (P = 0.99), and training with RJ (P = 0.94) had no significant effect on BDNF and training (P = 0.99) and training with RJ (P = 0.97) had no significant effect on NGF. Conclusions: It appears that RJ has a significant effect on the increase of NGF gene expression in the hippocampus tissue of rats with AD. Nevertheless, RJ consumption simultaneously with swimming training has no significant effect on BDNF and NGF.

The Investigation of Simultaneous EEG and Eye Tracking Characteristics During Fixation Task in Mild Alzheimer’s Disease

2020 ◽  
pp. 155005942093275
Author(s):  
Malihe Moghadami ◽  
Sahar Moghimi ◽  
Ali Moghimi ◽  
Gholam Reza Malekzadeh ◽  
Javad Salehi Fadardi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Eye Tracking ◽  
Clinical Symptoms ◽  
Neurodegenerative Disorder ◽  
Control Group ◽  
Alpha Power ◽  
Fixational Eye Movements ◽  
Fixation Task ◽  
Fixation Frequency

Alzheimer’s disease (AD) is a neurodegenerative disorder that occurs many years before the first clinical symptoms. Finding more exact, significant, and valuable criteria or indices for the diagnosis of the mild form of Alzheimer’s disease is very important for clinical and research purposes. Electroencephalography (EEG) and eye tracking biomarkers would provide noninvasive tools for the early detection of AD. Due to the advantages of EEG and eye tracking, in this study, we employed them simultaneously to conduct research on the mild AD. For this purpose, 19 patients with mild AD were compared with 19 gender- and age-matched normal subjects who did not have any history of cognitive or neurological disorders. EEG and eye-tracking data were concurrently collected in both groups in a fixation task. Our results revealed that the total fixation duration was significantly shorter for the AD patients, but their fixation frequency was more than that of the controls. In addition, increased theta power and decreased alpha power were observed in the AD group. Interestingly, there was a statistically significant correlation between fixation frequency and alpha power in the parietal area in the control group. However, this connection was not statistically significant in the AD group. The findings also indicated an elevated coherence in the AD patients in the parieto-occipital area. It is assumed that the AD patients might use the neural compensational processes for the fixation state. This study provides evidence for the simultaneously EEG and eye-tracking changes in the areas, which are involved in the control of the fixational eye movements.

EFFECT OF DROTAVERINE, A PHOSPHODIESTERASE 4 INHIBITOR IN SCOPOLAMINE-INDUCED COGNITIVE IMPAIRMENT IN RATS

2020 ◽  
pp. 99-102
Author(s):  
KAYALVIZHI MK
Keyword(s):  
Smooth Muscle ◽  
Cognitive Impairment ◽  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Enhancing Effect ◽  
Group I ◽  
Y Maze ◽  
Significant Difference ◽  
Group Ii ◽  
Memory Enhancing

Objective: Cognitive impairment (CI) is a progressive neurodegenerative disorder and causes significant dementia in the elderly. Intracellular cyclic AMP (cAMP) signaling has been well established in the mediation of memory. Phosphodiesterases (PDEs) are enzymes that catalyze the hydrolysis of cAMP and/or cyclic GMP. Drotaverine is a novel non-anticholinergic smooth muscle antispasmodic which acts by inhibiting PDE-4. It is now clinically used in smooth muscle spasms (intestinal, biliary and renal colic, irritable bowel syndrome, uterine spasms, etc.) without anticholinergic side effects. Since Drotaverine has PDE4 inhibition property, its role in learning and memory was evaluated in this study and found that it has memory enhancing effect comparable with donepezil in scopolamine-induced CI in rats. Methods: Learning and memory were assessed with two behavioral models, namely, elevated plus maze (EPM) and Y maze. CI was produced by scopolamine. Rats were divided into five groups, Group I treated with normal saline, Group II treated with scopolamine, and Groups III, IV, and V were treated with donepezil, Drotaverine, and both, respectively. Results: The result analysis revealed significant differences in transfer latency in EPM performance between Groups III, IV, V and Group II (***p<0.001). The results of spontaneous alternation in Y maze show that there was a significant difference among all the treatments groups (p<0.001). Conclusion: Drotaverine has promising memory enhancing effect in CI induced by scopolamine in rats. Further clinical trials are needed to prove this finding which has been elicited in animal models.

scholarly journals Therapeutic Effect of Yi-Chi-Tsung-Ming-Tang on Amyloidβ1−40-Induced Alzheimer's Disease-Like Phenotype via an Increase of Acetylcholine and Decrease of Amyloidβ

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Chung-Hsin Yeh ◽  
Ming-Tsuen Hsieh ◽  
Chi-Mei Hsueh ◽  
Chi-Rei Wu ◽  
Yi-Chun Huang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oral Administration ◽  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Senile Dementia ◽  
High Dose ◽  
Memory Impairments ◽  
Beneficial Role ◽  
Amyloid Accumulation

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by amyloid accumulation, neuronal death, and cognitive impairments. Yi-Chi-Tsung-Ming-Tang (YCTMT) is a traditional Chinese medicine and has never been used to enhance cognitive function and treat neurodegenerative disorders such as senile dementia. Whether YCTMT has a beneficial role in improving learning and memory in AD patients remains unclear. The present study showed that oral administration of YCTMT ameliorated amyloid-β- (Aβ1−40) injection-induced learning and memory impairments in rats, examined using passive avoidance and Morris water-maze tests. Immunostaining and Western Blot results showed that continuous Aβ1−40infusion caused amyloid accumulation and decreased acetylcholine level in hippocampus. Oral administration of medium and high dose of YCTMT 7 days after the Aβ1−40infusion decreased amyloid accumulation area and reversed acetylcholine decline in the Aβ1−40-injected hippocampus, suggesting that YCTMT might inhibit Aβplague accumulation and rescue reduced acetylcholine expression. This study has provided evidence on the beneficial role of YCTMT in ameliorating amyloid-induced AD-like symptom, indicating that YCTMT may offer an alternative strategy for treating AD.

scholarly journals Electroacupuncture Improves Clearance of Amyloid-β through the Glymphatic System in the SAMP8 Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Pei-zhe Liang ◽  
Li Li ◽  
Ya-nan Zhang ◽  
Yan Shen ◽  
Li-li Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Control Group ◽  
Nissl Staining ◽  
Glymphatic System ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

Background. Memory loss and cognitive impairment characterize the neurodegenerative disorder, Alzheimer’s disease (AD). Amyloid-β (Aβ) is the key factor that triggers the course of AD, and reducing the deposition of Aβ in the brain has been considered as a potential target for the treatment of AD. In clinical and animal studies, electroacupuncture (EA) has been shown to be an effective treatment for AD. In recent years, substantial evidence has accumulated suggesting the important role of the glymphatic system in Aβ clearance. Objective. The purpose of this study was to explore whether EA modifies the accumulation of Aβ through the glymphatic system and may thus be applied to alleviate cognitive impairments. Methods. Seven-month-old SAMP8 mice were randomized into a control group (Pc) and an electroacupuncture group (Pe). Age-matched SAMR1 mice were used as normal controls (Rc). Mice in the Pe group were stimulated on Baihui (GV20) and Yintang (GV29) for 10 min and then pricked at Shuigou (GV26) for ten times. EA treatment lasted for 8 weeks. In each week, EA would be applied once a day for the first five consecutive days and ceased at the remaining two days. After EA treatment, Morris water maze (MWM) test was used to evaluate the cognitive function; HE and Nissl staining was performed to observe the brain histomorphology; ELISA, contrast-enhanced MRI, and immunofluorescence were applied to explore the mechanisms underlying EA effects from Aβ accumulation, glymphatic system function, reactivity of astrocytes, and AQP4 polarization, respectively. Results. This EA regime could improve cognition and alleviate neuropathological damage to brain tissue. And EA treatment might reduce Aβ accumulation, enhance paravascular influx in the glymphatic system, inhibit the reactivity of astrocytes, and improve AQP4 polarity. Conclusion. EA treatment might reduce Aβ accumulation from the brain via improving clearance performance of the glymphatic system and thereby alleviating cognitive impairment.

Receptor-Interacting Protein Kinase 1 (RIPK1) as a Potential Therapeutic Target: An Overview of Its Possible Role in the Pathogenesis of Alzheimer's Disease

2019 ◽  
Vol 16 (10) ◽  
pp. 907-918
Author(s):  
Hong Hao Chan ◽  
Rhun Yian Koh ◽  
Chooi Ling Lim ◽  
Chee Onn Leong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Kinase ◽  
Neurodegenerative Disorder ◽  
Psychiatric Symptoms ◽  
Current Treatment ◽  
Interacting Protein ◽  
Amyloid Aβ ◽  
Cognition Impairment ◽  
Insight Into

Alzheimer’s Disease (AD) is an age-dependent neurodegenerative disorder, the most common type of dementia that is clinically characterized by the presence of beta-amyloid (Aβ) extracellularly and intraneuronal tau protein tangles that eventually leads to the onset of memory and cognition impairment, development of psychiatric symptoms and behavioral disorders that affect basic daily activities. Current treatment approved by the U.S Food and Drug Administration (FDA) for AD is mainly focused on the symptoms but not on the pathogenesis of the disease. Recently, receptor-interacting protein kinase 1 (RIPK1) has been identified as a key component in the pathogenesis of AD through necroptosis. Furthermore, genetic and pharmacological suppression of RIPK1 has been shown to revert the phenotype of AD and its mediating pathway is yet to be deciphered. This review is aimed to provide an overview of the pathogenesis and current treatment of AD with the involvement of autophagy as well as providing a novel insight into RIPK1 in reverting the progression of AD, probably through an autophagy machinery.

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

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