scholarly journals Selenomethionine Ameliorates Cognitive Impairment, Decreases Hippocampal Oxidative Stress and Attenuates Dysbiosis in D-Galactose-Treated Mice

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 111
Author(s):  
Ying Gao ◽  
Yongquan Xu ◽  
Junfeng Yin
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Morris Water Maze Test ◽  
Taxonomic Structure ◽  
Avoidance Task ◽  
Older Individuals ◽  
Object Recognition Test ◽  
Age Related ◽  
Structure Correlations ◽  
Α Diversity

The prevalence of age-related cognitive impairment is increasing as the proportion of older individuals in the population grows. It is therefore necessary and urgent to find agents to prevent or ameliorate age-related cognitive impairment. Selenomethionine (SeMet) is a natural amino acid occurring in yeast and Brazil nuts. It mitigates cognitive impairment in an Alzheimer’s disease mouse model, however, whether it works on age-related cognitive impairment remains unknown. In this study, SeMet significantly improved the performance of D-galactose-treated mice in the novel object recognition test, passive avoidance task and Morris water maze test. SeMet reversed D-galactose-induced reduction of hippocampal acetylcholine levels, suppression of choline acetyltransferase activity and activation of acetyl cholinesterase. It decreased D-galactose-induced oxidative stress and increased the selenoprotein P levels in the hippocampus. Besides, it attenuated D-galactose-induced dysbiosis by increasing the α-diversity and modulating the taxonomic structure. Correlations between certain taxa and physiological parameters were observed. Our results provide evidence of the effectiveness of SeMet on ameliorating D-galactose-induced cognitive impairment and suggest SeMet has potential to be used in the prevention or adjuvant treatment of age-related cognitive impairment.

scholarly journals Effects of Pueraria candollei var mirifica (Airy Shaw and Suvat.) Niyomdham on Ovariectomy-Induced Cognitive Impairment and Oxidative Stress in the Mouse Brain

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3442
Author(s):  
Yaowared Chulikhit ◽  
Wichitsak Sukhano ◽  
Supawadee Daodee ◽  
Waraporn Putalun ◽  
Rakvajee Wongpradit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Morris Water Maze Test ◽  
Object Recognition Test ◽  
Pueraria Mirifica ◽  
Beneficial Effects ◽  
Maze Test ◽  
Y Maze ◽  
Tnf Α ◽  
17Β Estradiol

The effects of the phytoestrogen-enriched plant Pueraria mirifica (PM) extract on ovari-ectomy (OVX)-induced cognitive impairment and hippocampal oxidative stress in mice were investigated. Daily treatment with PM and 17β-estradiol (E2) significantly elevated cognitive behavior as evaluated by using the Y maze test, the novel object recognition test (NORT), and the Morris water maze test (MWM), attenuated atrophic changes in the uterus and decreased serum 17β-estradiol levels. The treatments significantly ameliorated ovariectomy-induced oxidative stress in the hippocampus and serum by a decrease in malondialdehyde (MDA), an enhancement of superoxide dismutase, and catalase activity, including significantly down-regulated expression of IL-1β, IL-6 and TNF-α proinflammatory cytokines, while up-regulating expression of PI3K. The present results suggest that PM extract suppresses oxidative brain damage and dysfunctions in the hippocampal antioxidant system, including the neuroinflammatory system in OVX animals, thereby preventing OVX-induced cognitive impairment. The present results indicate that PM exerts beneficial effects on cognitive deficits for which menopause/ovariectomy have been implicated as risk factors.

scholarly journals Cirsium japonicum var. Maackii Improves Cognitive Impairment under Amyloid Beta25-35-Induced Alzheimer’s Disease Model

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Qi Qi Pang ◽  
Ji-Hyun Kim ◽  
Ji Myung Choi ◽  
Jia-Le Song ◽  
Sanghyun Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Object Recognition ◽  
Ethyl Acetate Fraction ◽  
Morris Water Maze Test ◽  
Dependent Manner ◽  
Object Recognition Test ◽  
Cirsium Japonicum

Abnormal production and degradation of amyloid beta (Aβ) in the brain lead to oxidative stress and cognitive impairment in Alzheimer’s disease (AD). Cirsium japonicum var. maackii (CJM) is widely used as an herbal medicine and has antibacterial and anti-inflammatory properties. This study focused on the protective effect of the ethyl acetate fraction from CJM (ECJM) on Aβ25-35-induced control mice. In the T-maze and novel object recognition test, ECJM provided higher spatial memory and object recognition compared to Aβ25-35 treatment alone. In the Morris water maze test, ECJM-administered mice showed greater learning and memory abilities than Aβ25-35-induced control mice. Additionally, ECJM-administered mice experienced inhibited lipid peroxidation and nitric oxide production in a dose-dependent manner. The present study indicates that ECJM improves cognitive impairment by inhibiting oxidative stress in Aβ25-35-induced mice. Therefore, CJM may be useful for the treatment of AD and may be a potential material for functional foods.

scholarly journals Age-related cognitive impairment is associated with long-term neuroinflammation and oxidative stress in a mouse model of episodic systemic inflammation

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Joana Costa d’Avila ◽  
Luciana Domett Siqueira ◽  
Aurélien Mazeraud ◽  
Estefania Pereira Azevedo ◽  
Debora Foguel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Systemic Inflammation ◽  
Age Related ◽  
And Oxidative Stress

scholarly journals Mild Cognitive Impairment or Attention-Deficit/Hyperactivity Disorder in Older Adults? A Cross Sectional Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Felippe Mendonca ◽  
Felipe Kenji Sudo ◽  
Gustavo Santiago-Bravo ◽  
Natalia Oliveira ◽  
Naima Assuncao ◽  
...  
Keyword(s):  
Attention Deficit Hyperactivity Disorder ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Attention Deficit ◽  
Cross Sectional Study ◽  
Older Individuals ◽  
Sectional Study ◽  
Cross Sectional ◽  
Hyperactivity Disorder ◽  
Age Related

Background: Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly prevalent neurodevelopmental condition, which may be associated with life-enduring cognitive dysfunction. It has been hypothesized that age-related cognitive decline may overlap with preexisting deficits in older ADHD patients, leading to increased problems to manage everyday-life activities. This phenomenon may mimic neurodegenerative disorders, in particular Mild Cognitive Impairment (MCI). This cross-sectional study aims to assess cognitive and behavioral differences between older subjects with ADHD and MCI.Methods: A total of 107 older participants (41 controls; 40 MCI and 26 ADHD; mean age = 67.60 ± 7.50 years; mean schooling = 15.14 ± 2.77 years; 65.4% females) underwent clinical, cognitive, and behavioral assessments by a multidisciplinary team at the Memory Clinic, D'Or Institute for Research and Education, Rio de Janeiro, Brazil. Mean scores in neuropsychological tasks and behavioral scales were compared across groups.Results: Participants with ADHD showed poorer performances than controls in episodic memory and executive function with large effect-sizes. Performances were comparable between MCI and ADHD for all domains.Discussion: MCI and ADHD in older individuals are dissociated clinical entities with overlapping cognitive profiles. Clinicians ought to be aware of these converging phenotypes to avoid misdiagnosis.

scholarly journals Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment

2019 ◽  
Vol 316 (5) ◽  
pp. H1124-H1140 ◽  
Author(s):  
Gabor A. Fulop ◽  
Stefano Tarantini ◽  
Andriy Yabluchanskiy ◽  
Andrea Molnar ◽  
Calin I. Prodan ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Arteries ◽  
Vascular Cognitive Impairment ◽  
Cerebral Veins ◽  
Older Individuals ◽  
Low Velocity ◽  
Venous Circulation ◽  
Age Related ◽  
The Brain

There has been an increasing appreciation of the role of vascular contributions to cognitive impairment and dementia (VCID) associated with old age. Strong preclinical and translational evidence links age-related dysfunction and structural alterations of the cerebral arteries, arterioles, and capillaries to the pathogenesis of many types of dementia in the elderly, including Alzheimer’s disease. The low-pressure, low-velocity, and large-volume venous circulation of the brain also plays critical roles in the maintenance of homeostasis in the central nervous system. Despite its physiological importance, the role of age-related alterations of the brain venous circulation in the pathogenesis of vascular cognitive impairment and dementia is much less understood. This overview discusses the role of cerebral veins in the pathogenesis of VCID. Pathophysiological consequences of age-related dysregulation of the cerebral venous circulation are explored, including blood-brain barrier disruption, neuroinflammation, exacerbation of neurodegeneration, development of cerebral microhemorrhages of venous origin, altered production of cerebrospinal fluid, impaired function of the glymphatics system, dysregulation of cerebral blood flow, and ischemic neuronal dysfunction and damage. Understanding the age-related functional and phenotypic alterations of the cerebral venous circulation is critical for developing new preventive, diagnostic, and therapeutic approaches to preserve brain health in older individuals.

scholarly journals Dexamethasone Treatment Reverses Cognitive Impairment but Increases Brain Oxidative Stress in Rats Submitted to Pneumococcal Meningitis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Tatiana Barichello ◽  
Ana Lucia B. Santos ◽  
Cintia Silvestre ◽  
Jaqueline S. Generoso ◽  
Andreza L. Cipriano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Pneumococcal Meningitis ◽  
Inhibitory Avoidance ◽  
Protein Carbonyl ◽  
Avoidance Task ◽  
Mitochondrial Superoxide ◽  
Neurologic Sequelae ◽  
Brain Oxidative Stress ◽  
And Oxidative Stress

Pneumococcal meningitis is associated with a significant mortality rate and neurologic sequelae. The animals received either 10 μL of saline or aS. pneumoniaesuspension and were randomized into different groups: sham: placebo with dexamethasone 0.7 mg/kg/1 day; placebo with dexamethasone 0.2 mg/kg/7 days; meningitis groups: dexamethasone 0.7 mg/kg/1 day and dexamethasone 0.2 mg/kg/7 days. Ten days after induction we evaluated memory and oxidative stress parameters in hippocampus and cortex. In the step-down inhibitory avoidance task, we observed memory impairment in the meningitis group with dexamethasone 0.2 mg/kg/7 days. The lipid peroxidation was increased in hippocampus in the meningitis groups with dexamethasone and in cortex only in the meningitis group with dexamethasone 0.2 mg/kg/7 days. The protein carbonyl was increased in hippocampus in the meningitis groups with dexamethasone and in cortex in the meningitis groups with and without dexamethasone. There was a decrease in the proteins integrity in hippocampus in all groups receiving treatment with dexamethasone and in cortex in all groups with dexamethasone (0.7 mg/kg/1 day). The mitochondrial superoxide was increased in the hippocampus and cortex in the meningitis group with dexamethasone 0.2 mg/kg/7 days. Our findings demonstrate that dexamethasone reverted cognitive impairment but increased brain oxidative stress in hippocampus and cortex in Wistar rats ten days after pneumococcal meningitis induction.

scholarly journals FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2/HO-1 Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-21 ◽  
Author(s):  
Ting Wan ◽  
Zihao Wang ◽  
Yi Luo ◽  
Yifan Zhang ◽  
Wei He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Caffeic Acid ◽  
Cell Apoptosis ◽  
Nuclear Translocation ◽  
Neurodegenerative Disorder ◽  
Neuronal Cell ◽  
Caffeic Acid Phenethyl Ester ◽  
Therapeutic Drug ◽  
Age Related

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder with cognitive deficits, which is becoming markedly more common in the world. Currently, the exact cause of AD is still unclear, and no curative therapy is available for preventing or mitigating the disease progression. Caffeic acid phenethyl ester (CAPE), a natural phenolic compound derived from honeybee hive propolis, has been reported as a potential therapeutic agent against AD, while its application is limited due to the low water solubility and poor bioavailability. Here, caffeic acid phenethyl ester 4-O-glucoside (FA-97) is synthesized. We validate that FA-97 attenuates H2O2-induced apoptosis in SH-SY5Y and PC12 cells and suppresses H2O2-induced oxidative stress by inhibiting the ROS level, malondialdehyde (MDA) level, and protein carbonylation level, as well as induces cellular glutathione (GSH) and superoxide dismutase (SOD). Mechanistically, FA-97 promotes the nuclear translocation and transcriptional activity of Nrf2 associated with the upregulated expression of HO-1 and NQO-1. The prime importance of Nrf2 activation in the neuroprotective and antioxidant effects of FA-97 is verified by Nrf2 siRNA transfection. In addition, FA-97 prevents scopolamine- (SCOP-) induced learning and memory impairments in vivo via reducing neuronal apoptosis and protecting against cholinergic system dysfunction in the hippocampus and cortex. Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2. In conclusion, FA-97 protects against oxidative stress-mediated neuronal cell apoptosis and SCOP-induced cognitive impairment by activating Nrf2/HO-1 signaling, which might be developed as a therapeutic drug for AD.

scholarly journals Krill Oil Attenuates Cognitive Impairment by the Regulation of Oxidative Stress and Neuronal Apoptosis in an Amyloid β-Induced Alzheimer’s Disease Mouse Model

Molecules ◽  
2020 ◽  
Vol 25 (17) ◽  
pp. 3942
Author(s):  
Ji Hyun Kim ◽  
Hui Wen Meng ◽  
Mei Tong He ◽  
Ji Myung Choi ◽  
Dongjun Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Neuronal Apoptosis ◽  
Morris Water Maze Test ◽  
Krill Oil ◽  
Cognitive Improvement ◽  
The Brain

In the present study, we investigated the cognitive improvement effects and its mechanisms of krill oil (KO) in Aβ25–35-induced Alzheimer’s disease (AD) mouse model. The Aβ25–35-injected AD mouse showed memory and cognitive impairment in the behavior tests. However, the administration of KO improved novel object recognition ability and passive avoidance ability compared with Aβ25–35-injected control mice in behavior tests. In addition, KO-administered mice showed shorter latency to find the hidden platform in a Morris water maze test, indicating that KO improved learning and memory abilities. To evaluate the cognitive improvement mechanisms of KO, we measured the oxidative stress-related biomarkers and apoptosis-related protein expressions in the brain. The administration of KO inhibited oxidative stress-related biomarkers such as reactive oxygen species, malondialdehyde, and nitric oxide compared with AD control mice induced by Aβ25–35. In addition, KO-administered mice showed down-regulation of Bax/Bcl-2 ratio in the brain. Therefore, this study indicated that KO-administered mice improved cognitive function against Aβ25–35 by attenuations of neuronal oxidative stress and neuronal apoptosis. It suggests that KO might be a potential agent for prevention and treatment of AD.

scholarly journals The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition

2021 ◽  
Vol 22 (7) ◽  
pp. 3574
Author(s):  
Aleksandra Kaliszewska ◽  
Joseph Allison ◽  
Matteo Martini ◽  
Natalia Arias
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Diseases ◽  
Lifestyle Factor ◽  
Aging Brain ◽  
Late Adulthood ◽  
Age Related ◽  
Age Related Cognitive Decline

Aging is inevitable and it is one of the major contributors to cognitive decline. However, the mechanisms underlying age-related cognitive decline are still the object of extensive research. At the biological level, it is unknown how the aging brain is subjected to progressive oxidative stress and neuroinflammation which determine, among others, mitochondrial dysfunction. The link between mitochondrial dysfunction and cognitive impairment is becoming ever more clear by the presence of significant neurological disturbances in human mitochondrial diseases. Possibly, the most important lifestyle factor determining mitochondrial functioning is nutrition. Therefore, with the present work, we review the latest findings disclosing a link between nutrition, mitochondrial functioning and cognition, and pave new ways to counteract cognitive decline in late adulthood through diet.

scholarly journals Functional vascular contributions to cognitive impairment and dementia: mechanisms and consequences of cerebral autoregulatory dysfunction, endothelial impairment, and neurovascular uncoupling in aging

2017 ◽  
Vol 312 (1) ◽  
pp. H1-H20 ◽  
Author(s):  
Peter Toth ◽  
Stefano Tarantini ◽  
Anna Csiszar ◽  
Zoltan Ungvari
Keyword(s):  
Cognitive Impairment ◽  
Experimental Studies ◽  
The Elderly ◽  
Neuronal Dysfunction ◽  
Older Individuals ◽  
Blood Brain Barrier Disruption ◽  
Vasomotor Function ◽  
Age Related ◽  
Brain Barrier Disruption ◽  
Cerebral Microhemorrhages

Increasing evidence from epidemiological, clinical and experimental studies indicate that age-related cerebromicrovascular dysfunction and microcirculatory damage play critical roles in the pathogenesis of many types of dementia in the elderly, including Alzheimer’s disease. Understanding and targeting the age-related pathophysiological mechanisms that underlie vascular contributions to cognitive impairment and dementia (VCID) are expected to have a major role in preserving brain health in older individuals. Maintenance of cerebral perfusion, protecting the microcirculation from high pressure-induced damage and moment-to-moment adjustment of regional oxygen and nutrient supply to changes in demand are prerequisites for the prevention of cerebral ischemia and neuronal dysfunction. This overview discusses age-related alterations in three main regulatory paradigms involved in the regulation of cerebral blood flow (CBF): cerebral autoregulation/myogenic constriction, endothelium-dependent vasomotor function, and neurovascular coupling responses responsible for functional hyperemia. The pathophysiological consequences of cerebral microvascular dysregulation in aging are explored, including blood-brain barrier disruption, neuroinflammation, exacerbation of neurodegeneration, development of cerebral microhemorrhages, microvascular rarefaction, and ischemic neuronal dysfunction and damage. Due to the widespread attention that VCID has captured in recent years, the evidence for the causal role of cerebral microvascular dysregulation in cognitive decline is critically examined.

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