scholarly journals Hesperidin Reduces Memory Impairment Associated with Adult Rat Hippocampal Neurogenesis Triggered by Valproic Acid

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4364
Author(s):  
Anusara Aranarochana ◽  
Soraya Kaewngam ◽  
Tanaporn Anosri ◽  
Apiwat Sirichoat ◽  
Wanassanun Pannangrong ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Memory Impairment ◽  
Memory Loss ◽  
Hippocampal Neurogenesis ◽  
Immunofluorescent Staining ◽  
Ki 67 ◽  
Novel Object ◽  
Memory Impairments ◽  
Adult Rat ◽  
Behavioral Expression

Treatment with valproic acid (VPA) deteriorates hippocampal neurogenesis, which leads to memory impairment. Hesperidin (Hsd) is a plant-based bioflavonoid that can augment learning and memory. This study aimed to understand the effect of Hsd on the impairment of hippocampal neurogenesis and memory caused by VPA. The VPA (300 mg/kg) was administered by intraperitoneal injection twice daily for 14 days, and Hsd (100 mg/kg/day) was administered by oral gavage once a day for 21 days. All rats underwent memory evaluation using the novel object location (NOL) and novel object recognition (NOR) tests. Immunofluorescent staining of Ki-67, BrdU/NeuN, and doublecortin (DCX) was applied to determine hippocampal neurogenesis in cell proliferation, neuronal survival, and population of the immature neurons, respectively. VPA-treated rats showed memory impairments in both memory tests. These impairments resulted from VPA-induced decreases in the number of Ki-67-, BrdU/NeuN-, and DCX-positive cells in the hippocampus, leading to memory loss. Nevertheless, the behavioral expression in the co-administration group was improved. After receiving co-administration with VPA and Hsd, the numbers of Ki-67-, BrdU/NeuN-, and DCX-positive cells were improved to the normal levels. These findings suggest that Hsd can reduce the VPA-induced hippocampal neurogenesis down-regulation that results in memory impairments.

Protective effects of melatonin against valproic acid-induced memory impairments and reductions in adult rat hippocampal neurogenesis

Neuroscience ◽  
2019 ◽  
Vol 406 ◽  
pp. 580-593 ◽  
Author(s):  
Anusara Aranarochana ◽  
Pornthip Chaisawang ◽  
Apiwat Sirichoat ◽  
Wanassanun Pannangrong ◽  
Peter Wigmore ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Hippocampal Neurogenesis ◽  
Protective Effects ◽  
Memory Impairments ◽  
Adult Rat

scholarly journals Hesperidin Alleviates Methotrexate-Induced Memory Deficits via Hippocampal Neurogenesis in Adult Rats

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 936 ◽  
Author(s):  
Salinee Naewla ◽  
Apiwat Sirichoat ◽  
Wanassanan Pannangrong ◽  
Pornthip Chaisawang ◽  
Peter Wigmore ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Memory Loss ◽  
Memory Deficits ◽  
Hippocampal Neurogenesis ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Ki 67 ◽  
Novel Object ◽  
Immature Neurons

Methotrexate (MTX), a folic acid antagonist, is widely used in cancer treatment. However, treatment with MTX reduces hippocampal neurogenesis, leading to memory deficits. Hesperidin (Hsd) is a flavonoid glycoside that promotes anti-inflammation, acts as an antioxidant, and has neuroprotective properties. Consumption of Hsd enhances learning and memory. In the present study, we investigated the protective effects of Hsd against MTX-induced impairments of memory and neurogenesis; male Sprague Dawley rats were administered with a single dose of MTX (75 mg/kg) by intravenous (i.v.) injection on days 8 and 15 or Hsd (100 mg/kg) by oral gavage for 21 days. Memory was tested using novel object location (NOL) and novel object recognition (NOR) tasks. Immunofluorescence staining of Ki-67, bromodeoxyuridine (BrdU), and doublecortin (DCX) was performed to assess cell proliferation, survival, and immature neurons. The data showed that Hsd and MTX did not disable locomotor ability. The MTX animals exhibited memory deficits in both memory tests. There were significant decreases in the numbers of cell proliferation, survival, and immature neurons in the MTX animals. However, co-administration with MTX and Hsd alleviated memory loss and neurogenesis decline. These results revealed that Hsd could protect against MTX side effects in the animals in this study.

scholarly journals Phytoestrogenα-Zearalanol Improves Memory Impairment and Hippocampal Neurogenesis in Ovariectomized Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Yilong Dong ◽  
Aimei Jiang ◽  
Hongju Yang ◽  
Huicheng Chen ◽  
Yanmei Wang
Keyword(s):  
Postmenopausal Women ◽  
Memory Impairment ◽  
Memory Performance ◽  
Positive Control ◽  
Hippocampal Neurogenesis ◽  
Spatial Learning And Memory ◽  
Memory Impairments ◽  
Memory Protection ◽  
Ovariectomized Mice ◽  
Newborn Neurons

Estrogen is known to provide robust protection of memory in postmenopausal women, but the fact that estrogen may increase the incidence of uterine and breast tumors has undoubtedly limited the clinical use of estrogen. In the present study, the effect ofα-zearalanol (α-ZAL), a plant-derived phytoestrogen with low side-effect on uterine and breast, on memory has been evaluated in ovariectomized (OVX) mice when using 17β-estradiol (17β-E2) as an estrogen positive control. Our findings demonstrated that OVX resulted in impaired spatial learning and memory and reduced numbers of newborn neurons in the dentate gyrus of the hippocampus, while 17β-E2 orα-ZAL treatment significantly improved memory performance and restored hippocampal neurogenesis. We also found the reduction of brain derived neurotrophic factor (BDNF) and TrkB expression in OVX mice, which were ameliorated by 17β-E2 orα-ZAL supplementation. These results indicated thatα-ZAL may improve memory impairments induced by OVX and modulate the expression of BDNF-TrkB benefit to neurogenesis which may be involved in the memory protection fromα-ZAL, in a manner similar to that of 17β-E2. The present findings suggested thatα-ZAL may be a plausible substitute of 17β-E2 in improving memory in postmenopausal women.

scholarly journals Melatonin Ameliorates Valproic Acid-Induced Neurogenesis Impairment: The Role of Oxidative Stress in Adult Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Anusara Aranarochana ◽  
Apiwat Sirichoat ◽  
Wanassanun Pannangrong ◽  
Peter Wigmore ◽  
Jariya Umka Welbat
Keyword(s):  
Oxidative Stress ◽  
Valproic Acid ◽  
Memory Impairment ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Related Factor ◽  
Adult Rats ◽  
Anticonvulsant Medication ◽  
Circadian Physiology

Background. Valproic acid (anticonvulsant medication) has been found to inhibit histone deacetylase activity and suppress hippocampal neurogenesis, which causes memory impairment in both humans and rodents. The neurohormone melatonin, which regulates mammalian seasonal and circadian physiology, has recently been shown to have neuroprotective properties, counteracting memory impairment associated with VPA-caused hippocampal neurogenesis reduction. This study is aimed at investigating the molecular mechanisms of melatonin associated with VPA-induced hippocampal neurogenesis and memory impairment. Methods. Male Spraque-Dawley rats received VPA (300 mg/kg) twice daily or melatonin (8 mg/kg/day) or some rats were given melatonin for 14 days during VPA administration. Results. The VPA-treated rats showed a significant increase in malondialdehyde (MDA) levels in the hippocampus and p21-positive cells in the subgranular zone (SGZ) of the dentate gyrus (DG) but decreased superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities. Moreover, VPA significantly decreased levels of nestin, Notchl, nuclear factor erythroid 2-related factor 2 (Nrf2), doublecortin (DCX), sex determining region Y-box 2 (SOX2), and brain-derived neurotrophic factor (BDNF). Conclusions. We found that melatonin was able to counteract these neurotoxic effects, acting as a neuroprotectant in VPA-induced memory hippocampal neurogenesis impairment by preventing intracellular oxidative stress and increasing antioxidant activity.

scholarly journals Early Hippocampal Sharp-Wave Ripple Deficits Predict Later Learning and Memory Impairments in an Alzheimer’s Disease Mouse Model

2019 ◽  
Author(s):  
Emily A. Jones ◽  
Anna K. Gillespie ◽  
Seo Yeon Yoon ◽  
Loren M. Frank ◽  
Yadong Huang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Genetic Risk ◽  
Memory Impairment ◽  
Memory Loss ◽  
Memory Deficits ◽  
Power Reduction ◽  
Memory Impairments ◽  
Sharp Wave

SUMMARYAlzheimer’s disease (AD) is characterized by progressive memory loss, and there is a pressing need to identify early pathophysiological alterations that predict subsequent memory impairment. Hippocampal sharp-wave ripples (SWRs) – electrophysiological signatures of memory reactivation in the hippocampus – are a compelling candidate for doing so. Mouse models of AD show reductions in both SWR abundance and associated slow gamma (SG) power during aging, but these alterations have yet to be directly linked to memory impairments. In aged apolipoprotein E4 knock in (apoE4-KI) mice – a model of the major genetic risk factor for AD – we found that reduced SWR abundance and associated CA3 SG power predicted spatial memory impairments measured 1–2 months later. Importantly, SWR-associated CA3 SG power reduction in young apoE4-KI mice also predicted spatial memory deficits measured 10 months later. These results establish features of SWRs as potential functional biomarkers of memory impairment in AD.

scholarly journals Modification of NO-cGMP Pathway Differentially Affects Diazepam- and Flunitrazepam-Induced Spatial and Recognition Memory Impairments in Rodents

2019 ◽  
Vol 37 (4) ◽  
pp. 1036-1046 ◽  
Author(s):  
Jolanta Orzelska-Górka ◽  
Piotr Bernat ◽  
Piotr Tutka ◽  
Joanna Listos ◽  
Ewa Kędzierska ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Recognition Memory ◽  
Animal Behavior ◽  
Memory Impairment ◽  
Elevated Plus Maze ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Memory Impairments ◽  
Plus Maze ◽  
Cgmp Pathway

AbstractThis study investigated the influence of sildenafil and methylene blue (MB), two modulators of the nitric oxide (NO)-cyclic guanosine-3′,5′-monophosphate (cGMP) pathway on amnesic effects of two benzodiazepines (BZs) (diazepam (DZ) and flunitrazepam (FNZ)), in rodents—mice and rats. In the modified elevated plus maze (mEPM) and novel object recognition (NOR) tests, MB given ip at a dose of 5 mg/kg 5 min prior to DZ administration (0.25 or 1 mg/kg, sc) enhanced/induced memory impairment caused by DZ. When MB (2.5, 5, and 10 mg/kg) was applied 5 min prior to FNZ administration (0.05 and 0.1 mg/kg), an effect was opposite and memory impairment induced by FNZ was reduced. When sildenafil (2.5 and 5 mg/kg, ip) was applied 5 min prior to DZ, we observed a reduction of DZ-induced memory deficiency in the mEPM test. A similar effect of sildenafil was shown in the NOR test when the drug was applied at doses of 1.25, 2.5, and 5 mg/kg prior to DZ. In the mEPM test, sildenafil at abovementioned doses had no effects on FNZ-induced memory impairment. In turns, sildenafil administered at doses of 2.5 and 5 mg/kg increased the effect of FNZ on memory impairment in the NOR test. In conclusion, the NO-cGMP pathway is involved differentially into BZs-induced spatial and recognition memory impairments assessed using the NOR and mEPM tests. Modulators of the NO-cGMP pathway affect animal behavior in these tests in a different way depending on what benzodiazepine is applied.

scholarly journals Chrysin Protects against Memory and Hippocampal Neurogenesis Depletion in D-Galactose-Induced Aging in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1100
Author(s):  
Ram Prajit ◽  
Nataya Sritawan ◽  
Kornrawee Suwannakot ◽  
Salinee Naewla ◽  
Anusara Aranarochana ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Survival ◽  
Brain Aging ◽  
Cell Damage ◽  
Neuronal Cell ◽  
Hippocampal Neurogenesis ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Novel Object ◽  
Immature Neurons

The interruption of hippocampal neurogenesis due to aging impairs memory. The accumulation of D-galactose (D-gal), a monosaccharide, induces brain aging by causing oxidative stress and inflammation, resulting in neuronal cell damage and memory loss. Chrysin, an extracted flavonoid, has neuroprotective effects on memory. The present study aimed to investigate the effect of chrysin on memory and hippocampal neurogenesis in brains aged using D-gal. Male Sprague-Dawley rats received either D-gal (50 mg/kg) by i.p. injection, chrysin (10 or 30 mg/kg) by oral gavage, or D-gal (50 mg/kg) and chrysin (10 or 30 mg/kg) for 8 weeks. Memory was evaluated using novel object location (NOL) and novel object recognition (NOR) tests. Hippocampal neurogenesis was evaluated using Ki-67, 5-bromo-2′-deoxyuridine (BrdU), and doublecortin (DCX) immunofluorescence staining to determine cell proliferation, cell survival, and number of immature neurons, respectively. We found that D-gal administration resulted in memory impairment as measured by NOL and NOR tests and in depletions in cell proliferation, cell survival, and immature neurons. However, co-treatment with chrysin (10 or 30 mg/kg) attenuated these impairments. These results suggest that chrysin could potentially minimize memory and hippocampal neurogenesis depletions brought on by aging.

The Relationship Between Brain Fog and Medication Adherence for Individuals With Hypothyroidism

2021 ◽  
pp. 105477382110381
Author(s):  
Kelly Haskard-Zolnierek ◽  
Courtney Wilson ◽  
Julia Pruin ◽  
Rebecca Deason ◽  
Krista Howard
Keyword(s):  
Memory Impairment ◽  
Hormone Replacement ◽  
Long Term Memory ◽  
Adherence Level ◽  
Thyroid Hormone Replacement ◽  
Memory Impairments ◽  
Cognitive Failures ◽  
Short And Long Term ◽  
The Relationship

Individuals with hypothyroidism suffer from symptoms including impairments to cognition (i.e., “brain fog”). Medication can help reduce symptoms of hypothyroidism; however, brain fog may hinder adherence. The aim of this study was to determine if memory impairment and cognitive failures are related to treatment nonadherence in 441 individuals with hypothyroidism. Participants with a diagnosis of hypothyroidism and currently prescribed a thyroid hormone replacement medication were placed in two groups according to adherence level and compared on validated scales assessing impairments to memory and cognition. Results indicated a significant association between treatment nonadherence and self-reported brain fog, represented by greater cognitive and memory impairments. Nonadherent individuals indicated impairments with prospective, retrospective, and short- and long-term memory; and more cognitive failures, compared to adherent individuals. Findings suggest the importance of interventions to enhance adherence for individuals with brain fog, such as encouraging the use of reminders.

scholarly journals Amelioration of Scopolamine-Induced Learning and Memory Impairment byα-Pinene in C57BL/6 Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Gil-Yong Lee ◽  
Chan Lee ◽  
Gyu Hwan Park ◽  
Jung-Hee Jang
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Manganese Superoxide Dismutase ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Memory Loss ◽  
Cholinergic Neurons ◽  
Morris Water Maze Test ◽  
Heme Oxygenase 1 ◽  
Related Factor

Increasing evidence suggests that neurodegenerative disorders such as Alzheimer’s disease (AD) are mediated via disruption of cholinergic neurons and enhanced oxidative stress. Therefore, attention has been focused on searching for antioxidant phytochemicals for the prevention and/or treatment of AD through their ability to fortify cholinergic function and antioxidant defense capacity. In this study, we have investigated the neuroprotective effect ofα-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.), a muscarinic receptor antagonist in C57BL/6 mice. Administration of APN (10 mg/kg, i.p.) significantly improved SCO-induced cognitive dysfunction as assessed by Y-maze and passive avoidance tests. In Morris water-maze test, APN effectively shortened the mean escape latency to find the hidden platform during training days. To further elucidate the molecular mechanisms underlying the neuroprotective effect of APN, the expression of proteins involved in the acetylcholine metabolism and antioxidant system was examined. Particularly, APN treatment increased mRNA expression of choline acetyltransferase in the cortex and protein levels of antioxidant enzymes such as heme oxygenase-1 and manganese superoxide dismutase in the hippocampus via activation of NF-E2-related factor 2. These findings suggest the possible neuroprotective potentials of APN for the management of dementia with learning and memory loss.

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