scholarly journals Acupuncture Stimulation Alleviates Corticosterone-Induced Impairments of Spatial Memory and Cholinergic Neurons in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Bombi Lee ◽  
Bong-Jun Sur ◽  
Sunoh Kwon ◽  
Euntaek Jung ◽  
Insop Shim ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Water Maze ◽  
Escape Latency ◽  
Cholinergic Neurons ◽  
Male Rats ◽  
Neuroprotective Activity ◽  
Once Daily ◽  
Acupuncture Stimulation ◽  
Stimulation Of

The purpose of this study was to examine whether acupuncture improves spatial cognitive impairment induced by repeated corticosterone (CORT) administration in rats. The effect of acupuncture on the acetylcholinergic system was also investigated in the hippocampus. Male rats were subcutaneously injected with CORT (5 mg/kg) once daily for 21 days. Acupuncture stimulation was performed at the HT7 (Sinmun) acupoint for 5 min before CORT injection. HT7 acupoint is located at the end of transverse crease of ulnar wrist of forepaw. In CORT-treated rats, reduced spatial cognitive function was associated with significant increases in plasma CORT level (+36%) and hippocampal CORT level (+204%) compared with saline-treated rats. Acupuncture stimulation improved the escape latency for finding the platform in the Morris water maze. Consistently, the acupuncture significantly alleviated memory-associated decreases in cholinergic immunoreactivity and mRNA expression of BDNF and CREB in the hippocampus. These findings demonstrate that stimulation of HT7 acupoint produced significant neuroprotective activity against the neuronal impairment and memory dysfunction.

scholarly journals Association between tea consumption and cognitive impairment in middle-aged and older adults

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jia Zhang ◽  
Anxin Wang ◽  
Xiaoli Zhang ◽  
Shuohua Chen ◽  
Shouling Wu ◽  
...  
Keyword(s):  
Older Adults ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Green Tea ◽  
High Frequency ◽  
Epidemiological Studies ◽  
Neuroprotective Activity ◽  
Tea Consumption ◽  
Older Individuals ◽  
Middle Aged

Abstract Background Biologic studies have suggested that tea may have neuroprotective activity. However, tea’s protective effect on cognitive function is controversial in human epidemiological studies, and no data, including the middle-aged, are available. The objective of this study was to investigate the association of habit, frequency, and types of tea consumption with incident cognitive impairment in middle-aged and older adults. Methods Data from the Asymptomatic Polyvascular Abnormalities in Community study were used (aged over 40y). We gathered information on tea consumption, including habit, frequency, and types, via a standardized questionnaire and assessed cognitive function by Mini-Mental State Examination (MMSE) and/or Montreal Cognitive Assessment (MoCA). Three thousand eight hundred sixty-eight and 806 participants were selected in MMSE and MoCA subgroups. Multivariate logistic regression models were utilized to examine associations between tea consumption and cognitive impairment in middle-aged and older participants. Results In MMSE analyses, after adjustment for potential confounding factors, habitual (odds ratio (OR) 0.47, [95% confidence interval (CI) 0.33–0.68], p < 0.001) and high frequency (p trend < 0.001) of tea intake were associated with a lower risk of cognitive impairment. The risk of cognitive impairment was lower in green tea consumption (OR 0.36, [95% CI 0.22–0.61], p < 0.001) than other types (OR 0.59, [95% CI 0.38–0.91], p = 0.017). In MoCA analyses, we got similar results. Conclusions Habitual tea consumption, especially high-frequency and green tea consumption, was significantly associated with a lower prevalence of cognitive impairment in middle-aged and older individuals.

scholarly journals Effect of Evodia rutaecarpa (Juss) Benth extract on Alzheimer disease in mice

2020 ◽  
Vol 19 (4) ◽  
pp. 823-828
Author(s):  
Ang Cai ◽  
Liu Xiao ◽  
Yan-Ping Zhou ◽  
Zhi-Guo Zhang ◽  
Quan-Wei Yang
Keyword(s):  
Cognitive Function ◽  
Alzheimer Disease ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Evodia Rutaecarpa ◽  
Mouse Hippocampus

Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in the animals treated with 400 mg/kg ERBE (20.5 ± 1.3 s) was significantly higher than untreated 3xTg-AD mice (12.4 ± 1.3 s, p < 0.01). In addition, ERBE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.4 ± 0.2, p < 0.05) and TrkB (1.1 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: The results suggest that ERBE administration may be a useful strategy for treating memory impairment induced by several neurodegenerative diseases. Keywords: Evodia rutaecarpa, Alzheimer, Memory impairment, NeuN-positive cells

scholarly journals Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice

2021 ◽  
Vol 18 (9) ◽  
pp. 1903-1907
Author(s):  
Cen Su ◽  
Ping Niu ◽  
Yao-ming Xu ◽  
Ye Feng ◽  
Hai-ping Xia
Keyword(s):  
Cognitive Function ◽  
Protective Effect ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Immunohistochemical Assay ◽  
Maze Test ◽  
Acorus Tatarinowii

Purpose: To investigate the protective effect of Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice. Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in animals treated with 600 mg/kg ATE (24.8 ± 1.3 s) was significantly increased relative to ontreated 3xTg-AD mice (8.5 ± 1.0 s, p < 0.01). In addition, ATE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF (1.9 ± 0.4, p < 0.05) and TrkB (1.9 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: These results suggest that ATE treatment may be a useful strategy for managing memory impairment induced by several neurodegenerative diseases.

Abstract 146: Inducible Conditional Deletion of Dicer in Neural Progenitor Cells Induces Cognitive Impairment

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Rui Lan Zhang ◽  
Michael Chopp ◽  
Wanlong Pan ◽  
Xiaoming Zhang ◽  
Xianshuang Liu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Progenitor Cells ◽  
Morris Water Maze ◽  
Adult Neurogenesis ◽  
Water Maze ◽  
Oligodendrocyte Progenitor Cells ◽  
Cognitive Tests ◽  
Conditional Deletion

Background: MicroRNAs regulate adult neurogenesis. Conditional deletion of Dicer in neural stem cells (NSCs) causes postnatal death. The functional role of Dicer in adult neurogenesis remains unknown. Using mice with inducible conditional knock-down of Dicer in adult NSCs, we investigated the effect of ablation of Dicer on neurogenesis and cognitive function. Methods and Results: Young adult Ascl1-CreER:Dicerflox/flox mice (Dicer Cko, n= 32) were administered (i.p) with tamoxifen daily for 5 consecutive days and age matched wild-type litters (n= 30) were used as control. The mice were sacrificed at 2, 14 or 30 days after injection. Immunstaining was performed to detect phenotypes of subventricular zone (SVZ) cells. An array of cognitive tests including Morris Water Maze, odor-based novelty recognition, and sociability test were performed. Primary NPCs were isolated from the SVZ for vitro studies. Compared to control, Dicer CKo had 54% reduction of Dicer protein in NPCs. Cognitive tests showed that CKo spent 35% less time in the correct quadrant (p<0.05) of Morris Water Maze, significantly reduced time exploring new odor objects, 44 ±10% (p<0.05) in Cko animals compared with 77 ±10% in control, and significantly less time with other mice when they encountered a strange mouse during the sociability test (70 ± 9 vs 118 ±7 seconds, p<0.05). CKo significantly (p<0.05) reduced BrdU+ (16±2% vs 24±3%), and Ki67+ NPCs (25±3% vs 33±3%), doublecortin (DCX)+ neuroblasts (2± 0.6% vs 6± 1%), and Ng2+ oligodendrocyte progenitor cells (OPCs, 8±1% vs 12± 2%) in the SVZ. However, Dicer CKo animals exhibited a significant increase (p<0.05) of apoptotic NPCs (14±0.5% vs 10 ±0.3%). These in vivo findings were consistent with data from cultured NPCs. Dicer CKo also showed significant (p<0.05) reduction DCX+ neuroblasts in the rostral migratory stream and APC+ mature oligodendrocytes in the corpus callosum. Conclusion: Our data demonstrated that inducible conditional ablation of Dicer in Ascl1 lineage NPCs impairs neurogenesis and oligodendrogenesis in adult SVZ niche and white matter, and induces cognitive impairment, indicating that Dicer in adult NPCs is essential for maintaining neurogenesis and oligodendrogenesis and is important for cognitive function.

scholarly journals Mechanism of Autonomic Exercise Improving Cognitive Function of Alzheimer’s Disease by Regulating lncRNA SNHG14

2021 ◽  
Vol 36 ◽  
pp. 153331752110276
Author(s):  
Yuchen He ◽  
Yi Qiang
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Transgenic Mice ◽  
Cognitive Ability ◽  
Escape Latency ◽  
Cognitive Disorder ◽  
Qrt Pcr ◽  
Test Elisa ◽  
Tnf Α ◽  
Double Transgenic Mice

This paper studied the influence of exercise on the cognitive ability of AD patients and elucidated potential mechanisms. The expression of SNHG14 was validated by qRT-PCR. The cognitive impairment of mice was examined by MWM Test. ELISA tests were applied to discover the influence of SNHG14 on inflammation. Overexpression of SNHG14 was found in AD patients and underexpression of SNHG14 was identified in these AD patients after exercise. In APP/PS1 double transgenic mice, SNHG14 reversed the protective impacts of exercise on escape latency and distance moved. The upregulation of SNHG14 also inhibited the effects of exercise on the percentage of time spent in the target quadrant and times of platform crossing. Besides, overexpression of SNHG14 reversed the repressed expression of IL-6, IL-1β, and TNF-α. In total, exercise could ameliorate cognitive disorder and inflammation activity by reducing the levels of SNHG14.

scholarly journals Improvement of cognitive impairment in female type 2 diabetes mellitus mice by spironolactone

2011 ◽  
Vol 13 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Akiko Sakata ◽  
Masaki Mogi ◽  
Jun Iwanami ◽  
Kana Tsukuda ◽  
Li-Juan Min ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Kkay Mice

Patients with type 2 diabetes mellitus (T2DM) exhibit more severe cognitive decline in females compared with males; however, the preventive approach to this gender-specific cognitive decline is still an enigma. Spironolactone is a potassium-sparing diuretic that also acts as an androgen receptor antagonist. Here, we investigated whether spironolactone attenuates cognitive impairment observed in female T2DM mice. Adult wild-type (WT) mice and an obese T2DM model, KKAy mice, were employed in this study. Cognitive function was evaluated by the shuttle avoidance test and Morris water maze test. Administration of spironolactone (50 mg/kg per day in chow) had no significant effect on blood pressure, glucose tolerance or insulin resistance. In WT mice, no significant sex difference in cognitive function was observed; however, treatment with spironolactone improved spatial memory in the water maze, especially in female WT mice. Administration of spironolactone markedly improved the cognitive decline in female KKAy mice up to the level in male KKAy mice. Spironolactone treatment also improved cognitive function in ovariectomized-KKAy mice, but failed to improve it in those with administration of estradiol (200 µg/kg per day). In diabetic mice, spironolactone improved impaired cognitive function observed in female mice, suggesting that spironolactone may prevent cognitive impairment associated with diabetes in females clinically.

scholarly journals Ameliorating Effects of Ethanol Extract ofFructus mumeon Scopolamine-Induced Memory Impairment in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Min-Soo Kim ◽  
Won Kyung Jeon ◽  
Kye Wan Lee ◽  
Yu Hwa Park ◽  
Jung-Soo Han
Keyword(s):  
Cognitive Function ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Impairment ◽  
Cholinergic Neurons ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Memory Impairments ◽  
Morris Water Maze Task ◽  
Increased Activity

We previously reported thatFructus mume(F. mume) extract shows protective effects on memory impairments and anti-inflammatory effects induced by chronic cerebral hypoperfusion. Neurodegeneration of basal cholinergic neurons is also observed in the brain with chronic cerebral hypoperfusion. Therefore, the present study was conducted to examine whetherF. mumeextracts enhance cognitive function via the action of cholinergic neuron using a scopolamine-induced animal model of memory impairments.F. mume(50, 100, or 200 mg/kg) was administered to C57BL/6 mice for 14 days (days 1–14) and memory impairment was induced by scopolamine (1 mg/kg), a muscarinic receptor antagonist for 7 days (days 8–14). Spatial memory was assessed using Morris water maze and hippocampal level of acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) was examined by ELISA and immunoblotting. Mice that received scopolamine alone showed impairments in acquisition and retention in Morris water maze task and increased activity of AChE in the hippocampus. Mice that receivedF. mumeand scopolamine showed no scopolamine-induced memory impairment and increased activity of AChE. In addition, treatments ofF. mumeincreased ChAT expression in the hippocampus. These results indicated thatF. mumemight enhance cognitive function via action of cholinergic neurons.

scholarly journals Rosuvastatin Improves Cognitive Function of Chronic Hypertensive Rats by Attenuating White Matter Lesions and Beta-Amyloid Deposits

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Lu Zheng ◽  
Ying Cai ◽  
Baoshan Qiu ◽  
Linfang Lan ◽  
Jing Lin ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Object Recognition ◽  
Cognitive Function ◽  
White Matter ◽  
Water Maze ◽  
Novel Object Recognition ◽  
Hypertensive Rats ◽  
Object Recognition Test ◽  
Novel Object ◽  
Novel Object Recognition Test

Hypertensive white matter lesion (WML) is one of common causes of vascular cognitive impairment. In this study, we aimed to investigate the effect of rosuvastatin on cognitive impairment and its underlying mechanisms in chronic hypertensive rats. From the 8th week after establishment of stroke-prone renovascular hypertensive rats (RHRSPs), rosuvastatin (10 mg/kg) or saline as a control was administrated once daily for consecutive 12 weeks by gastric gavage. Cognitive function was assessed with the Morris water maze test and novel object recognition test. WML was observed by Luxol fast blue staining. Aβ deposits, Claudin-5, Occludin, and ZO-1 were determined by immunofluorescence. After rosuvastatin treatment, the escape latencies were decreased and the time of crossing the hidden platform was increased in the Morris water maze, compared with the vehicle-treated RHRSP group. In a novel object recognition test, the recognition index in the rosuvastatin-treated RHRSP group was significantly larger than that in the vehicle-treated RHRSP group. Rosuvastatin treatment presented with the effects of lower WML grades, higher expression of tight junction proteins Claudin-5, Occludin, and ZO-1 in the corpus callosum, and less Aβ deposits in the cortex and hippocampus. The data suggested that rosuvastatin improved the cognitive function of chronic hypertensive rats partly by attenuating WML and reducing Aβ burden.

Effect of Obesity on Cognitive Impairment in Vascular Dementia Rat Model via BDNF-ERK-CREB Pathway

2020 ◽  
pp. 109980042095163
Author(s):  
Yoonju Kim ◽  
Youn-Jung Kim
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Vascular Dementia ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Male Rats ◽  
Creb Pathway

The prevalence of vascular dementia continues to increase with no cure. Thus, it is important identify the aggravating factors of vascular dementia to delay disease progression in patients. Obesity is a well-known risk factor for vascular dementia and causes mild cognitive impairment. In the present study, we evaluated whether obesity exacerbates cognitive impairment in vascular dementia rats and how it affects synaptic plasticity through the BDNF pathway. We randomly assigned 30 Wistar male rats to three groups: sham surgery (Sham), vascular dementia (VaD), and vascular dementia with obesity (OB + VaD). We fed rats a 60% high-fat diet to establish obesity; we then induced vascular dementia using bilateral common carotid artery occlusion. After 6 weeks, we evaluated cognitive function using the Morris water maze and radial arm maze tests. We analyzed post-synaptic density-95 (PSD95) and growth-associated protein-43 (GAP43) to confirm synaptic plasticity. We also evaluated brain-derived neurotrophic factor (BDNF), phosphorylated extracellular signal-regulated kinase (pERK), and phosphorylated cyclic adenosine monophosphate response element-binding protein (pCREB) in the hippocampus. The OB + VaD group showed the most impaired cognitive function on behavioral tests, with decreases in PSD95. The VaD group showed increased levels of BDNF, pERK, and pCREB, while the OB + VaD group displayed decreased levels. We suggest that obesity exacerbates cognitive impairment in vascular dementia by inhibiting the compensatory increases of BDNF-ERK-CREB pathway.

scholarly journals Characterization of age-related changes in synaptic transmission onto F344 rat basal forebrain cholinergic neurons using a reduced synaptic preparation

2014 ◽  
Vol 111 (2) ◽  
pp. 273-286 ◽  
Author(s):  
William H. Griffith ◽  
Dustin W. DuBois ◽  
Annette Fincher ◽  
Kathryn A. Peebles ◽  
Jennifer L. Bizon ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Basal Forebrain ◽  
Water Maze ◽  
Cholinergic Neurons ◽  
Cognitive Status ◽  
Synaptic Function ◽  
Male Rats ◽  
Patch Clamp Recording ◽  
Age Related

Basal forebrain (BF) cholinergic neurons participate in a number of cognitive processes that become impaired during aging. We previously found that age-related enhancement of Ca2+ buffering in rat cholinergic BF neurons was associated with impaired performance in the water maze spatial learning task (Murchison D, McDermott AN, Lasarge CL, Peebles KA, Bizon JL, and Griffith WH. J Neurophysiol 102: 2194–2207, 2009). One way that altered Ca2+ buffering could contribute to cognitive impairment involves synaptic function. In this report we show that synaptic transmission in the BF is altered with age and cognitive status. We have examined the properties of spontaneous postsynaptic currents (sPSCs) in cholinergic BF neurons that have been mechanically dissociated without enzymes from behaviorally characterized F344 rats. These isolated neurons retain functional presynaptic terminals on their somata and proximal dendrites. Using whole cell patch-clamp recording, we show that sPSCs and miniature PSCs are predominately GABAergic (bicuculline sensitive) and in all ways closely resemble PSCs recorded in a BF in vitro slice preparation. Adult (4–7 mo) and aged (22–24 mo) male rats were cognitively assessed using the water maze. Neuronal phenotype was identified post hoc using single-cell RT-PCR. The frequency of sPSCs was reduced during aging, and this was most pronounced in cognitively impaired subjects. This is the same population that demonstrated increased intracellular Ca2+ buffering. We also show that increasing Ca2+ buffering in the synaptic terminals of young BF neurons can mimic the reduced frequency of sPSCs observed in aged BF neurons.

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