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 Naloxone Ameliorates Spatial Memory Deficits and Hyperthermia Induced by a Neurotoxic Methamphetamine Regimen in Male Rats

2019 ◽  
Vol 8 ◽  
pp. 1182 ◽  
Author(s):  
Solmaz Khalifeh ◽  
Mehdi Khodamoradi ◽  
Vahid Hajali ◽  
Hamed Ghazvini ◽  
Lelia Eliasy ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Spatial Memory ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Impairment ◽  
Memory Performance ◽  
Poor Performance ◽  
Male Rats ◽  
Spatial Learning And Memory ◽  
Opiate Antagonist

Background: Methamphetamine (METH) as a synthetic psychostimulant is being increasingly recognized as a worldwide problem, which may induce memory impairment. On the other hand, it is well established that naloxone, an opiate antagonist, has some beneficial effects on learning and memory. The present research aimed at evaluating naloxone effects on spatial learning and memory impairment triggered by a neurotoxic regimen of METH in male rats. Materials and Methods: The animals received the subcutaneous (sc) regimen of METH (4×6 mg/kg at 2-h intervals), intraperitoneal (ip) naloxone (4×1 mg/kg at 2-h intervals), or normal saline at four events. The Nal-METH group of rats received four naloxone injections (1 mg/kg, ip) 30 min before each METH injection (6 mg/kg, sc) at 2-h intervals. Seven days later, they were evaluated for spatial learning and memory in the Morris Water Maze (MWM) task. Result: METH regimen induced hyperthermia, as well as a poor performance, in the acquisition and retention phases of the task, indicating spatial learning and memory impairment compared to the controls. Naloxone administration (1 mg/kg, ip) before each METH injection led to significant attenuations of both hyperthermia and METH adverse effects on the rat performance in the MWM task. Conclusion: The results revealed that pretreatment with the opiate antagonist naloxone could prevent METH adverse effects on body temperature and memory performance. It seems that the opioidergic system and hyperthermia may, at least partially, be involved in METH effects on spatial memory. [GMJ. 2019;8:e1182]

scholarly journals Evidence for a pervasive autobiographical memory impairment in Logopenic Progressive Aphasia: clinical and neural correlates

2020 ◽  
Author(s):  
Siddharth Ramanan ◽  
David Foxe ◽  
Hashim El-Omar ◽  
Rebekah M. Ahmed ◽  
John R. Hodges ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Autobiographical Memory ◽  
Memory Impairment ◽  
Language Disorder ◽  
Memory Performance ◽  
Memory Function ◽  
Structured Interview ◽  
Progressive Aphasia ◽  
Memory Impairments

ABSTRACTLogopenic Progressive Aphasia is a rare language disorder characterised by repetition and naming difficulties, reflecting the progressive degeneration of left-lateralized peri-sylvian temporal and inferior parietal regions. Mounting evidence suggests that cognitive impairments in this syndrome extend beyond the language domain to include episodic encoding and retrieval disturbances. To date, it remains unknown whether autobiographical memories from across the lifespan are also subject to decline, yet this information is critical to arrive at a comprehensive understanding of the Logopenic syndrome. The objective of this study was to provide the first in depth examination of autobiographical memory function in Logopenic Progressive Aphasia using the Autobiographical Interview, a validated semi-structured interview which assesses recollection of the past under free and probed recall conditions. Autobiographical memory performance in 10 well-characterised Logopenic Progressive Aphasia patients was contrasted with that of 18 typical amnestic Alzheimer’s disease and 16 healthy Control participants. Relative to Controls, Logopenic Progressive Aphasia cases showed marked impairment in the free recall of episodic details, scoring comparably to disease-matched cases of Alzheimer’s disease. This impairment was evident across all time periods and persisted even when formal structured probing was provided. Importantly, controlling for overall level of language disruption failed to ameliorate the autobiographical memory impairment in the Logopenic Progressive Aphasia group, suggesting a genuine amnesia spanning recent and remote memories. Whole-brain voxel-based morphometry analyses revealed that total episodic information retrieved in Logopenic Progressive Aphasia was associated with decreased grey matter intensity predominantly in a bilateral posterior parietal network. Taken together, our findings reveal for the first time the presence of marked remote and recent autobiographical memory impairments in Logopenic Progressive Aphasia, that cannot be explained solely due to their language difficulties or disease staging. Our findings hold important clinical implications for the accurate characterization of Logopenic Progressive Aphasia, and suggest that episodic memory difficulties should be considered as one of the core clinical features of this syndrome.

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.

ROLE(S) OF GRAVITATIONAL LOADING ON THE GROWTH AND DEVELOPMENT OF NEUROMUSCULAR PROPERTIES

2020 ◽  
Vol 54 (6) ◽  
pp. 73-79
Author(s):  
F. Kawano ◽  
◽  
T. Ohira ◽  
K. Goto ◽  
Y. Ohira ◽  
...  
Keyword(s):  
Motor Function ◽  
Growth And Development ◽  
Hippocampal Neurogenesis ◽  
Hindlimb Unloading ◽  
Hindlimb Suspension ◽  
Spatial Learning And Memory ◽  
Single Muscle ◽  
Memory Functions ◽  
Growing Period ◽  
Gravitational Loading

The roles of gravitational load or anti-gravitational muscular activities on the growth and development of motor function and/or anti-gravity muscle, soleus, had been investigated. In this review, the responses of growth-associated changes in swimming [1, 2] and/or surface righting performance [3], spatial learning and memory functions [4], and hippocampal neurogenesis [5] or protein expression [6] to hindlimb unloading (HU) by hindlimb suspension or spaceflight during neonatal growing period in rats were discussed. Effects on the morphological and contractile properties, distribution of neuromuscular junction in single muscle fibers, sampled from tendon-to-tendon, and roles of satellite cells and myonuclei in the regulation of these properties [7–9] were also reviewed.

Is adult hippocampal neurogenesis really relevant for the treatment of psychiatric disorders?

2020 ◽  
Vol 18 ◽  
Author(s):  
Marco Carli ◽  
Stefano Aringhieri ◽  
Shivakumar Kolachalam ◽  
Biancamaria Longoni ◽  
Giovanna Grenno ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Emotional Processing ◽  
Imaging Techniques ◽  
Hippocampal Neurogenesis ◽  
Adult Brain ◽  
Adult Hippocampal Neurogenesis ◽  
Mood Stabilizers ◽  
Post Traumatic Stress ◽  
Newborn Neurons ◽  
Hippocampal Circuitry

: Adult neurogenesis consists in the generation of newborn neurons from neural stem cells taking place in the adult brain. In mammals, this process is limited to very few areas of the brain, and one of these neurogenic niches is the subgranular layer of the dentate gyrus (DG) of the hippocampus. Adult newborn neurons are generated from quiescent neural progenitors (QNPs), which differentiate through different steps into mature granule cells (GCs), to be finally integrated into the existing hippocampal circuitry. In animal models, adult hippocampal neurogenesis (AHN) is relevant for pattern discrimination, cognitive flexibility, emotional processing and resilience to stressful situations. Imaging techniques allow to visualize newborn neurons within the hippocampus through all their stages of development and differentiation. In humans, the evidence of AHN is more challenging, and, based on recent findings, it persists through the adulthood, even if it declines with age. Whether this process has an important role in human brain function and how it integrates into the existing hippocampal circuitry is still a matter of exciting debate. Importantly, AHN deficiency has been proposed to be relevant in many psychiatric disorders, including mood disorders, anxiety, post-traumatic stress disorder and schizophrenia. This review aims to investigate how AHN is altered in different psychiatric conditions and how pharmacological treatments can rescue this process. In fact, many psychoactive drugs, such as antidepressants, mood stabilizers and atypical antipsychotics (AAPs), can boost AHN with different results. In addition, some non-pharmacological approaches are discussed as well.

scholarly journals Silicon dioxide nanoparticles induced neurobehavioral impairments by disrupting microbiota–gut–brain axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jun Diao ◽  
Yinyin Xia ◽  
Xuejun Jiang ◽  
Jingfu Qiu ◽  
Shuqun Cheng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Health Risk ◽  
Silicon Dioxide ◽  
Spatial Learning And Memory ◽  
Rrna Gene ◽  
Silicon Dioxide Nanoparticles ◽  
Potential Health ◽  
Specific Chemical ◽  
Memory Impairments ◽  
Tissue Integrity

Abstract Background Silicon dioxide nanoparticles (SiO2NPs) are widely used as additive in the food industry with controversial health risk. Gut microbiota is a new and hot topic in the field of nanotoxicity. It also contributes a novel and insightful view to understand the potential health risk of food-grade SiO2NPs in children, who are susceptible to the toxic effects of nanoparticles. Methods In current study, the young mice were orally administrated with vehicle or SiO2NPs solution for 28 days. The effects of SiO2NPs on the gut microbiota were detected by 16S ribosomal RNA (rRNA) gene sequencing, and the neurobehavioral functions were evaluated by open field test and Morris water maze. The level of inflammation, tissue integrity of gut and the classical indicators involved in gut–brain, gut–liver and gut–lung axis were all assessed. Results Our results demonstrated that SiO2NPs significantly caused the spatial learning and memory impairments and locomotor inhibition. Although SiO2NPs did not trigger evident intestinal or neuronal inflammation, they remarkably damaged the tissue integrity. The microbial diversity within the gut was unexpectedly enhanced in SiO2NPs-treated mice, mainly manifested by the increased abundances of Firmicutes and Patescibacteria. Intriguingly, we demonstrated for the first time that the neurobehavioral impairments and brain damages induced by SiO2NPs might be distinctively associated with the disruption of gut–brain axis by specific chemical substances originated from gut, such as Vipr1 and Sstr2. Unapparent changes in liver or lung tissues further suggested the absence of gut–liver axis or gut–lung axis regulation upon oral SiO2NPs exposure. Conclusion This study provides a novel idea that the SiO2NPs induced neurotoxic effects may occur through distinctive gut–brain axis, showing no significant impact on either gut–lung axis or gut–liver axis. These findings raise the exciting prospect that maintenance and coordination of gastrointestinal functions may be critical for protection against the neurotoxicity of infant foodborne SiO2NPs.

scholarly journals Early stages of tau pathology and its associations with functional connectivity, atrophy and memory

Brain ◽  
2021 ◽  
Author(s):  
David Berron ◽  
Jacob W Vogel ◽  
Philip S Insel ◽  
Joana B Pereira ◽  
Long Xie ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Entorhinal Cortex ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Memory Impairment ◽  
Memory Performance ◽  
Hippocampal Atrophy ◽  
Tau Pathology ◽  
Β Amyloid ◽  
With Memory

Abstract In Alzheimer’s disease, postmortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with area 35, and the entorhinal cortex. Here we used tau-PET imaging to investigate the sequence of tau pathology progression within the human medial temporal lobe and across regions in the posterior-medial system. Our objective was to study how medial temporal tau is related to functional connectivity, regional atrophy, and memory performance. We included 215 β-amyloid negative cognitively unimpaired, 81 β-amyloid positive cognitively unimpaired and 87 β-amyloid positive individuals with mild cognitive impairment, who each underwent [18]F-RO948 tau and [18]F-flutemetamol amyloid PET imaging, structural T1-MRI and memory assessments as part of the Swedish BioFINDER-2 study. First, event-based modelling revealed that the entorhinal cortex and area 35 show the earliest signs of tau accumulation followed by the anterior and posterior hippocampus, area 36 and the parahippocampal cortex. In later stages, tau accumulation became abnormal in neocortical temporal and finally parietal brain regions. Second, in cognitively unimpaired individuals, increased tau load was related to local atrophy in the entorhinal cortex, area 35 and the anterior hippocampus and tau load in several anterior medial temporal lobe subregions was associated with distant atrophy of the posterior hippocampus. Tau load, but not atrophy, in these regions was associated with lower memory performance. Further, tau-related reductions in functional connectivity in critical networks between the medial temporal lobe and regions in the posterior-medial system were associated with this early memory impairment. Finally, in patients with mild cognitive impairment, the association of tau load in the hippocampus with memory performance was partially mediated by posterior hippocampal atrophy. In summary, our findings highlight the progression of tau pathology across medial temporal lobe subregions and its disease-stage specific association with memory performance. While tau pathology might affect memory performance in cognitively unimpaired individuals via reduced functional connectivity in critical medial temporal lobe-cortical networks, memory impairment in mild cognitively impaired patients is associated with posterior hippocampal atrophy.

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.

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