Scutellaria baicalensis stem-leaf total flavonoid might attenuate learning/memory impairment and neuronal loss in rats induced by amyloid beta-peptide. This study aimed to explore the effects of Scutellaria baicalensi...Scutellaria baicalensis stem-leaf total flavonoid might attenuate learning/memory impairment and neuronal loss in rats induced by amyloid beta-peptide. This study aimed to explore the effects of Scutellaria baicalensis stem-leaf total flavonoid on amyloid beta-peptide-induced neuronal apoptosis and the expression of apoptosis-related proteins in the rat hippocampus. Male Wistar rats were given intragastric administration of Scutellaria baicalensis stem-leaf total flavonoid, 50 or 100 mg/kg, once per day. On day 8 after administration, 10 pg amyloid beta-peptide （25-35） was injected into the bilateral hippocampus of rats to induce neuronal apoptosis. On day 20, hippocampal tissue was harvested and probed with the terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay. Scutellaria baicalensis stem-leaf total flavonoid at 50 and 100 mg/kg reduced neuronal apoptosis induced by amyloid beta-peptide （25-35） in the rat hippocampus. Immunohistochemistry and western blot assay revealed that expression of the pro-apoptotic protein Bax, cytochrome c and caspase-3 was significantly diminished by 50 and 100 mg/kg Scutellaria baicalensis stem-leaf total flavonoid, while expression of the anti-apoptotic protein Bcl-2 was increased. Moreover, 100 mg/kg Scutellana baicalensis stem-leaf total flavonoid had a more dramatic effect than the lower dosage. These experimental findings indicate that Scutellaria baicalensis stem-leaf total flavonoid dose-dependently attenuates neuronal apoptosis induced by amyloid beta-peptide in the hippocampus, and it might mediate this by regulating the expression of Bax, cytochrome c, caspase-3 and Bcl-2.展开更多
Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer＇s disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid ...Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer＇s disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide （25-35） （Aβ25-35）. In the present study, PC12 cells were cultured with different doses （0, 0.1, 1.0, 10 and 100 nmol/L） of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25-3s for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester （〉 10 nmol/L） prolonged the survival of PC12 cells after Aβ25-35 induction, decreased the expression of apoptosis-related proteins caspase-3, -8, -9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa B expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25-35-induced PC12 apoptosis.展开更多
OBJECTIVE: To examine the effects of Yokukansan(YKS) extract on two endogenous modulators of anxiety, brain-derived neurotrophic factor(BDNF)and serotonin (5-HT)_(2A) receptors pharmacologically, in the ischemic rat m...OBJECTIVE: To examine the effects of Yokukansan(YKS) extract on two endogenous modulators of anxiety, brain-derived neurotrophic factor(BDNF)and serotonin (5-HT)_(2A) receptors pharmacologically, in the ischemic rat model of dementia.METHODS: The cerebral ischemia(CI) was induced by bilateral occlusion of the vertebral and common carotid arteries(4-vessel occlusion ischemia). The CI was combined with the amyloid-β42 peptide(A42) injected intracerebroventricularly, and referreβdto as CI+Aβ. Anxiety-like behaviors were assessed by elevated plus maze(enclosed arm), light/dark transition test(dark chamber), and open-field test.Wet-dog shakes were induced by the 5-HT_(2A) receptor agonist 2, 5-dimethoxy-4-iodoamphetamine(DOI). The concentration of BDNF in serum was determined by enzyme-linked immuno sorbent assay.RESULTS: CI + Aβ increased anxiety, as demonstrated by the increase of time spent in the enclosed arms and dark chambers, and locomotion in the outer zone of the open field(thigmotaxis). CI + Adecreased the serum concentration of BDNF. YKS reβ-duced the anxiety-like behaviors, suppressed the DOI-induced wet-dog shakes and increased serum BDNF concentrations.CONCLUSION: Our findings suggest that YKS extract improves CI + Aβ-induced anxiety by antagonizing 5-HT_(2A) receptors and increasing BDNF.展开更多
Alzheimer's disease(AD)is a multifactorial neurodegenerative disorder characterized by the presence of senile plaques and neurofibrillary tangles.Research attempts to identify characteristic factors that are assoc...Alzheimer's disease(AD)is a multifactorial neurodegenerative disorder characterized by the presence of senile plaques and neurofibrillary tangles.Research attempts to identify characteristic factors that are associated with the presence of the AD pathology on the one hand and that increase the risk of developing AD on the other.Changes in non-rapid eye movement(NREM)sleep may meet both requirements for various reasons.First,NREM-sleep is important for optimal memory function.In addition,studies report that the presence of AD pathology is associated with NREM-sleep changes.Finally,more and more results appear to suggest that sleep problems are not only a symptom of AD but can also increase the risk of AD.Several of these studies suggest that it is primarily a lack of NREM-sleep that is responsible for this increased risk.However,the majority investigated sleep only through subjective reporting,as a result of which NREMsleep could not be analyzed separately.The aim of this literature study is therefore to present the results of the studies that relate the AD pathology and NREM-sleep(registered by electroencephalography).Furthermore,we try to evaluate whether NREM-sleep analysis could be used to support the diagnosis of AD and whether NREM-sleep deficiency could be a causal factor in the development of AD.展开更多
Background:Focused ultrasound(FUS)-mediated blood-brain barrier(BBB)opening has shown efficacy in removal of amyloid plaque and improvement of cognitive functions in preclinical studies,but this is rarely reported in ...Background:Focused ultrasound(FUS)-mediated blood-brain barrier(BBB)opening has shown efficacy in removal of amyloid plaque and improvement of cognitive functions in preclinical studies,but this is rarely reported in clinical studies.This study was conducted to evaluate the safety,feasibility and potential benefits of repeated extensive BBB opening.Methods:In this open-label,prospective study,six patients with Alzheimer's disease(AD)were enrolled at Severance Hospital in Korea between August 2020 and September 2020.Five of them completed the study.FUS-mediated BBB opening,targeting the bilateral frontal lobe regions over 20 cm^(3),was performed twice at three-month intervals.Magnetic resonance imaging,^(18)F-Florbetaben(FBB)positron emission tomography,Caregiver-Administered Neuropsychiatric Inventory(CGA-NPI)and comprehensive neuropsychological tests were performed before and after the procedures.Results:FUS targeted a mean volume of 21.1±2.7 cm^(3)and BBB opening was confirmed at 95.7%±9.4%of the targeted volume.The frontal-to-other cortical region FBB standardized uptake value ratio at 3 months after the procedure showed a slight decrease,which was statistically significant,compared to the pre-procedure value(-1.6%,0.986 vs 1.002,P=0.043).The CGA-NPI score at 2 weeks after the second procedure significantly decreased compared to baseline(2.2±3.0 vs 8.6±6.0,P=0.042),but recovered after 3 months(5.2±5.8 vs 8.6±6.0,P=0.89).No adverse effects were observed.Conclusions:The repeated and extensive BBB opening in the frontal lobe is safe and feasible for patients with AD.In addition,the BBB opening is potentially beneficial for amyloid removal in AD patients.展开更多
Background Recently, 1,5-dicaffeoylquinic acid （1,5-DQA）, a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have no...Background Recently, 1,5-dicaffeoylquinic acid （1,5-DQA）, a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have not yet been clearly identified. The purpose of this study was to explore the protective mechanisms of 1,5-DQA on neuronal culture. Methods We investigated the neuroprotective effects of 1,5-DQA against amyloid IB1-42 （Aβ42）-induced neurotoxicity in primary neuronal culture. To evaluate the neuroprotective effects of 1,5-DQA, primary cultured cortical neurons from neonate rats were pretreated with 1,5-DQA for 2 hours and then treated with 40 pmol/L Aβ42 for 6 hours. Cell counting kit-8, Hoechst staining and Western blotting were used for detecting the protective mechanism. Comparisons between two groups were evaluated by independent t test, and multiple comparisons were analyzed by one-way analysis of variance （ANOVA）. Results 1,5-DQA treated neurons showed increased neuronal cell viability against Aβ42 toxicity in a concentration- dependent manner, both phosphoinositide 3-kinase （PI3K）/Akt and extracellular regulated protein kinase 1/2 （Erkl/2） were activated by 1,5-DQA with stimulating their upstream tyrosine kinase A （Trk A）. However, the neuroprotective effects of 1,5-DQA were blocked by LY294002, a PI3K inhibitor, but not by PD98059, an inhibitor of mitogen-activated protein kinase kinase. Furthermore, 1,5-DQA＇s anti-apoptotic potential was related to the enhanced inactivating phosphorylation of glycogen synthase kinase 313 （GSK3β） and the modulation of expression of apoptosis-related protein Bcl-2/Bax. Conclusion These resutts suggest that 1,5-DQA prevents AI342-induced neurotoxicity through the activation of PI3K/Akt followed by the stimulation of Trk A, then the inhibition of GSK313 as well as the modulation of Bcl-2/Bax.展开更多
Comprehensive Summary Amyloid-β protein(Aβ)is a fatal cause of Alzheimer's disease,which can trigger a series of cytotoxicity by the abnormal aggregation of Aβ in human brain.The strategies for inhibition and d...Comprehensive Summary Amyloid-β protein(Aβ)is a fatal cause of Alzheimer's disease,which can trigger a series of cytotoxicity by the abnormal aggregation of Aβ in human brain.The strategies for inhibition and disaggregation of Aβ fibrillation are mostly based on the interaction between monomers,oligomers,fibrils,and materials.展开更多
Objective： To observe the effect of a Chinese medicine compound, Naoerkang （脑尔康, NEK）, on amyloid-beta peptide （1-42; A 131-42） and matrix metalloproteinase-9 （MMP-9） expressions in the hippocampus of AIzhei...Objective： To observe the effect of a Chinese medicine compound, Naoerkang （脑尔康, NEK）, on amyloid-beta peptide （1-42; A 131-42） and matrix metalloproteinase-9 （MMP-9） expressions in the hippocampus of AIzheimer＇s disease （AD） model rats. Methods： A total of 48 male Sprague Dawley （SD） rats were randomly divided into normal control, untreated, and piracetam groups, and low-dose, medium-dose, and high-dose NEK groups, with 8 rats in each group. The 5-1μL aggregated Aβ1-42 （2μg/μL） were injected into both CA1 areas of the hippocampus in the rats to establish an AD model, whereas the normal control was treated with the same dose of normal saline. The rats in the NEK groups were treated with a high, medium, or low dose of NEK [60 g/（kg-d）, 30 g/（kg-d）, and 15 g/（kg.d）], respectively, intragastrically for 28 days; piracetam （0.375 g/kg, intragastrically） was consecutively administered in the piracetam group; and normal saline was applied in the normal control and untreated groups. A Y-maze test was used for behavioral study to test the learning and memory abilities. A 131-~ and MMP-9 expressions in the hippocampus was determined immunohistochemically, and the results were analyzed by image acquisition and an analysis system. Results： Aggregated A 131.42 induced obvious learning and memory dysfunction, as well as up-regulation of A 13 1-42 expression in the hippocampus. Compared with those in the normal control group, the learning and memory abilities of rats in the untreated group significantly decreased （P〈0.01）, and the expression of A β1-42 was significantly increased （P〈0.01）. Twenty-eight days after different treatments, compared with those in the untreated group, the learning and memory abilities of AD model rats in the piracetam, low-dose, medium-dose and high-dose NEK groups were significantly improved （P〈0.01 or P〈0.05）, and the expression of Aβ1-42 in the hippocampus decreased （P〈0.01 or P〈0.05）, and MMP-9 increased （P〈0.01 or P〈0.05）, especially in the high-dose NEK group. Conclusion： NEK might play a role of anti-dementia by increasing the expression of MMP-9 in the hippocampus of AD model rats, resulting in the reduction of the quantity of Aβ1.42 and improvement in learning and memory ability in AD model rats.展开更多
基金supported by grants from Hebei Provincial Science and Technology Bureau,No.08276101D-21
文摘Scutellaria baicalensis stem-leaf total flavonoid might attenuate learning/memory impairment and neuronal loss in rats induced by amyloid beta-peptide. This study aimed to explore the effects of Scutellaria baicalensis stem-leaf total flavonoid on amyloid beta-peptide-induced neuronal apoptosis and the expression of apoptosis-related proteins in the rat hippocampus. Male Wistar rats were given intragastric administration of Scutellaria baicalensis stem-leaf total flavonoid, 50 or 100 mg/kg, once per day. On day 8 after administration, 10 pg amyloid beta-peptide （25-35） was injected into the bilateral hippocampus of rats to induce neuronal apoptosis. On day 20, hippocampal tissue was harvested and probed with the terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay. Scutellaria baicalensis stem-leaf total flavonoid at 50 and 100 mg/kg reduced neuronal apoptosis induced by amyloid beta-peptide （25-35） in the rat hippocampus. Immunohistochemistry and western blot assay revealed that expression of the pro-apoptotic protein Bax, cytochrome c and caspase-3 was significantly diminished by 50 and 100 mg/kg Scutellaria baicalensis stem-leaf total flavonoid, while expression of the anti-apoptotic protein Bcl-2 was increased. Moreover, 100 mg/kg Scutellana baicalensis stem-leaf total flavonoid had a more dramatic effect than the lower dosage. These experimental findings indicate that Scutellaria baicalensis stem-leaf total flavonoid dose-dependently attenuates neuronal apoptosis induced by amyloid beta-peptide in the hippocampus, and it might mediate this by regulating the expression of Bax, cytochrome c, caspase-3 and Bcl-2.
文摘Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer＇s disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide （25-35） （Aβ25-35）. In the present study, PC12 cells were cultured with different doses （0, 0.1, 1.0, 10 and 100 nmol/L） of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25-3s for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester （〉 10 nmol/L） prolonged the survival of PC12 cells after Aβ25-35 induction, decreased the expression of apoptosis-related proteins caspase-3, -8, -9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa B expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25-35-induced PC12 apoptosis.
文摘OBJECTIVE: To examine the effects of Yokukansan(YKS) extract on two endogenous modulators of anxiety, brain-derived neurotrophic factor(BDNF)and serotonin (5-HT)_(2A) receptors pharmacologically, in the ischemic rat model of dementia.METHODS: The cerebral ischemia(CI) was induced by bilateral occlusion of the vertebral and common carotid arteries(4-vessel occlusion ischemia). The CI was combined with the amyloid-β42 peptide(A42) injected intracerebroventricularly, and referreβdto as CI+Aβ. Anxiety-like behaviors were assessed by elevated plus maze(enclosed arm), light/dark transition test(dark chamber), and open-field test.Wet-dog shakes were induced by the 5-HT_(2A) receptor agonist 2, 5-dimethoxy-4-iodoamphetamine(DOI). The concentration of BDNF in serum was determined by enzyme-linked immuno sorbent assay.RESULTS: CI + Aβ increased anxiety, as demonstrated by the increase of time spent in the enclosed arms and dark chambers, and locomotion in the outer zone of the open field(thigmotaxis). CI + Adecreased the serum concentration of BDNF. YKS reβ-duced the anxiety-like behaviors, suppressed the DOI-induced wet-dog shakes and increased serum BDNF concentrations.CONCLUSION: Our findings suggest that YKS extract improves CI + Aβ-induced anxiety by antagonizing 5-HT_(2A) receptors and increasing BDNF.
基金Supported by the Funds Malou Malou,Perano,Georgette Paulus,JMJS Breugelmans and Gabrielle,François and Christian,Managed by the King Baudouin Foundation of Belgium,No.2021-J1990130-222081.
文摘Alzheimer's disease(AD)is a multifactorial neurodegenerative disorder characterized by the presence of senile plaques and neurofibrillary tangles.Research attempts to identify characteristic factors that are associated with the presence of the AD pathology on the one hand and that increase the risk of developing AD on the other.Changes in non-rapid eye movement(NREM)sleep may meet both requirements for various reasons.First,NREM-sleep is important for optimal memory function.In addition,studies report that the presence of AD pathology is associated with NREM-sleep changes.Finally,more and more results appear to suggest that sleep problems are not only a symptom of AD but can also increase the risk of AD.Several of these studies suggest that it is primarily a lack of NREM-sleep that is responsible for this increased risk.However,the majority investigated sleep only through subjective reporting,as a result of which NREMsleep could not be analyzed separately.The aim of this literature study is therefore to present the results of the studies that relate the AD pathology and NREM-sleep(registered by electroencephalography).Furthermore,we try to evaluate whether NREM-sleep analysis could be used to support the diagnosis of AD and whether NREM-sleep deficiency could be a causal factor in the development of AD.
基金supported by a grant from the Brain Research Program through the National Research Foundation of Korea(NRF)funded by the Korean Ministry of Science,ICT,Future Planning,a Government Department(2016M3C7A1914123).
文摘Background:Focused ultrasound(FUS)-mediated blood-brain barrier(BBB)opening has shown efficacy in removal of amyloid plaque and improvement of cognitive functions in preclinical studies,but this is rarely reported in clinical studies.This study was conducted to evaluate the safety,feasibility and potential benefits of repeated extensive BBB opening.Methods:In this open-label,prospective study,six patients with Alzheimer's disease(AD)were enrolled at Severance Hospital in Korea between August 2020 and September 2020.Five of them completed the study.FUS-mediated BBB opening,targeting the bilateral frontal lobe regions over 20 cm^(3),was performed twice at three-month intervals.Magnetic resonance imaging,^(18)F-Florbetaben(FBB)positron emission tomography,Caregiver-Administered Neuropsychiatric Inventory(CGA-NPI)and comprehensive neuropsychological tests were performed before and after the procedures.Results:FUS targeted a mean volume of 21.1±2.7 cm^(3)and BBB opening was confirmed at 95.7%±9.4%of the targeted volume.The frontal-to-other cortical region FBB standardized uptake value ratio at 3 months after the procedure showed a slight decrease,which was statistically significant,compared to the pre-procedure value(-1.6%,0.986 vs 1.002,P=0.043).The CGA-NPI score at 2 weeks after the second procedure significantly decreased compared to baseline(2.2±3.0 vs 8.6±6.0,P=0.042),but recovered after 3 months(5.2±5.8 vs 8.6±6.0,P=0.89).No adverse effects were observed.Conclusions:The repeated and extensive BBB opening in the frontal lobe is safe and feasible for patients with AD.In addition,the BBB opening is potentially beneficial for amyloid removal in AD patients.
文摘Background Recently, 1,5-dicaffeoylquinic acid （1,5-DQA）, a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have not yet been clearly identified. The purpose of this study was to explore the protective mechanisms of 1,5-DQA on neuronal culture. Methods We investigated the neuroprotective effects of 1,5-DQA against amyloid IB1-42 （Aβ42）-induced neurotoxicity in primary neuronal culture. To evaluate the neuroprotective effects of 1,5-DQA, primary cultured cortical neurons from neonate rats were pretreated with 1,5-DQA for 2 hours and then treated with 40 pmol/L Aβ42 for 6 hours. Cell counting kit-8, Hoechst staining and Western blotting were used for detecting the protective mechanism. Comparisons between two groups were evaluated by independent t test, and multiple comparisons were analyzed by one-way analysis of variance （ANOVA）. Results 1,5-DQA treated neurons showed increased neuronal cell viability against Aβ42 toxicity in a concentration- dependent manner, both phosphoinositide 3-kinase （PI3K）/Akt and extracellular regulated protein kinase 1/2 （Erkl/2） were activated by 1,5-DQA with stimulating their upstream tyrosine kinase A （Trk A）. However, the neuroprotective effects of 1,5-DQA were blocked by LY294002, a PI3K inhibitor, but not by PD98059, an inhibitor of mitogen-activated protein kinase kinase. Furthermore, 1,5-DQA＇s anti-apoptotic potential was related to the enhanced inactivating phosphorylation of glycogen synthase kinase 313 （GSK3β） and the modulation of expression of apoptosis-related protein Bcl-2/Bax. Conclusion These resutts suggest that 1,5-DQA prevents AI342-induced neurotoxicity through the activation of PI3K/Akt followed by the stimulation of Trk A, then the inhibition of GSK313 as well as the modulation of Bcl-2/Bax.
基金the financial support from the National Natural Science Foundation of China(Nos.21773054,21905072 and 22077025)the Natural Science Foundation of Hebei Province(Nos.B2020202062 and B2020202086).
文摘Comprehensive Summary Amyloid-β protein(Aβ)is a fatal cause of Alzheimer's disease,which can trigger a series of cytotoxicity by the abnormal aggregation of Aβ in human brain.The strategies for inhibition and disaggregation of Aβ fibrillation are mostly based on the interaction between monomers,oligomers,fibrils,and materials.
基金Supported by Tackle Key Problem in-Science and Technology Foundation of Shaanxi Province[No.2007K16-07(5)]
文摘Objective： To observe the effect of a Chinese medicine compound, Naoerkang （脑尔康, NEK）, on amyloid-beta peptide （1-42; A 131-42） and matrix metalloproteinase-9 （MMP-9） expressions in the hippocampus of AIzheimer＇s disease （AD） model rats. Methods： A total of 48 male Sprague Dawley （SD） rats were randomly divided into normal control, untreated, and piracetam groups, and low-dose, medium-dose, and high-dose NEK groups, with 8 rats in each group. The 5-1μL aggregated Aβ1-42 （2μg/μL） were injected into both CA1 areas of the hippocampus in the rats to establish an AD model, whereas the normal control was treated with the same dose of normal saline. The rats in the NEK groups were treated with a high, medium, or low dose of NEK [60 g/（kg-d）, 30 g/（kg-d）, and 15 g/（kg.d）], respectively, intragastrically for 28 days; piracetam （0.375 g/kg, intragastrically） was consecutively administered in the piracetam group; and normal saline was applied in the normal control and untreated groups. A Y-maze test was used for behavioral study to test the learning and memory abilities. A 131-~ and MMP-9 expressions in the hippocampus was determined immunohistochemically, and the results were analyzed by image acquisition and an analysis system. Results： Aggregated A 131.42 induced obvious learning and memory dysfunction, as well as up-regulation of A 13 1-42 expression in the hippocampus. Compared with those in the normal control group, the learning and memory abilities of rats in the untreated group significantly decreased （P〈0.01）, and the expression of A β1-42 was significantly increased （P〈0.01）. Twenty-eight days after different treatments, compared with those in the untreated group, the learning and memory abilities of AD model rats in the piracetam, low-dose, medium-dose and high-dose NEK groups were significantly improved （P〈0.01 or P〈0.05）, and the expression of Aβ1-42 in the hippocampus decreased （P〈0.01 or P〈0.05）, and MMP-9 increased （P〈0.01 or P〈0.05）, especially in the high-dose NEK group. Conclusion： NEK might play a role of anti-dementia by increasing the expression of MMP-9 in the hippocampus of AD model rats, resulting in the reduction of the quantity of Aβ1.42 and improvement in learning and memory ability in AD model rats.
