Repeated administration of almonds increases brain acetylcholine levels and enhances memory function in healthy rats while attenuates memory deficits in animal model of amnesia

Subarachnoid hemorrhage induces neuronal apoptosis which causes acute and long-term memory deficits. Ourhypothesis is that agonism of α7-acetylcholine receptors attenuates neuronal apoptosis and improves memorydeficits in SAH mice. Mice were randomly assigned into the experimental groups. One cohort was euthanizedone day after SAH to assess neuronal apoptosis and signaling pathways. A second cohort survived for 30 dayspost-SAH to test long-term memory function. Inhibitors and an α7-acetylcholine receptor knockout mouse wereused. Neurobehavioral performance was assessed on days 1-3, 5, 7, and 23-28. All outcomes were performedand all data was analyzed by a blinded investigator. The α7-acetylcholine receptor agonist prevented neuronalapoptosis and improved acute memory deficits caused by SAH via activation of the PI3K/Akt pathway in neurons.Agonism of the α7-acetylcholine receptor was beneficial in both male and female mice, although the protectionin females was significantly better than in male mice. α7-acetylcholine receptor agonism did not provide anybenefit in α7-acetylcholine receptor knockout mice subjected to SAH. Treatment with the α7-acetylcholinereceptor agonist for 3 days after SAH led to improved working memory one month after SAH suggesting thatacutely improving neuronal survival can have long-lasting benefits. The α7-acetylcholine receptor may be atherapeutic target for SAH which can promote neuronal survival acutely after SAH, but also confer long-lastingmemory benefits. The findings of this study support the α7-acetylcholine receptor as a treatment target whichmay attenuate the long-term memory deficits which SAH patients suffer from.

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Electroconvulsive therapy hasn’t negative effects on short-term memory function, as assessed using a bedside hand-held device

Mental Illness ◽

10.4081/mi.2017.7093 ◽

2017 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Helge H.O. Müller ◽

Mareen Reike ◽

Simon Grosse-Holz ◽

Mareike Röther ◽

Caroline Lücke ◽

...

Keyword(s):

Cognitive Performance ◽

Electroconvulsive Therapy ◽

Short Term Memory ◽

Memory Function ◽

Memory Deficits ◽

Treatment Resistant ◽

Negative Effects ◽

Short Term ◽

Term Memory ◽

Digital Measurements

Electroconvulsive therapy (ECT) is effective in the treatment of treatment-resistant major depression. The fear of cognitive impairment after ECT often deters patients from choosing this treatment option. There is little reliable information regarding the effects of ECT on overall cognitive performance, while short-term memory deficits are well known but not easy to measure within clinical routines. In this pilot study, we examined ECT recipients’ pre- and posttreatment performances on a digital ascending number tapping test. We found that cognitive performance measures exhibited good reproducibility in individual patients and that ECT did not significantly alter cognitive performance up to 2 hours after this therapy was applied. Our results can help patients and physicians make decisions regarding the administration of ECT. Digital measurements are recommended, especially when screening for the most common side effects on cognitive performance and short-term memory.

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Physical exercise and social interaction in complex environments reverse memory deficits induced by inhalants

Adaptive Behavior ◽

10.1177/1059712319854361 ◽

2019 ◽

Vol 27 (4) ◽

pp. 277-282

Author(s):

Roberto E Mercadillo ◽

Ricardo Mosco-Aquino ◽

Nayeli Páez-Martínez

Keyword(s):

Social Interaction ◽

Physical Exercise ◽

Environmental Enrichment ◽

Psychosocial Interventions ◽

Repeated Administration ◽

Memory Deficits ◽

Social Consequences ◽

Cognitive Stimulation ◽

Social Conditions ◽

Voluntary Exercise

Inhalant abuse is a global issue with major behavioral, cognitive, and social consequences. Some effects of this abuse are observed in memory deficits, but the organism–environment interactions are poorly understood. We propose that studying environmental enrichment (EE) in animal models allows the elucidation of adaptive behavior mechanisms to face harmful effects, as well as plausible translational interventions; however, the effects of the different elements that comprise the complexity of EE must be determined. In this work, we measured the effects of housing under five environments for 4 weeks on memory impairments induced by the repeated administration of toluene in mice (4000 ppm, 30 min/day for 4 weeks). Recognition memory was recovered after housing in a complete enriched environment involving voluntary exercise with running wheels, cognitive stimulation with objects to explore, and social interaction. However, enrichment with only voluntary exercise in social conditions produced a significant memory recovery. In addition, EE in isolation showed fewer beneficial effects, while cognitive stimulation, even under social conditions, did not reverse the memory impairment by itself. We argue that physical exercise and social interaction could derive in cognitive enhancement and be used to advise on psychosocial interventions.

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Human Neural Stem Cells Encoding ChAT Gene Restore Cognitive Function via Acetylcholine Synthesis, Aβ Elimination, and Neuroregeneration in APPswe/PS1dE9 Mice

International Journal of Molecular Sciences ◽

10.3390/ijms21113958 ◽

2020 ◽

Vol 21 (11) ◽

pp. 3958

Author(s):

Dongsun Park ◽

Ehn-Kyoung Choi ◽

Tai-Hyoung Cho ◽

Seong Soo Joo ◽

Yun-Bae Kim

Keyword(s):

Stem Cell ◽

Cognitive Function ◽

Memory Function ◽

Memory Deficits ◽

Therapeutic Approaches ◽

Human Neural Stem Cells ◽

Ache Inhibitors ◽

Human Neural Stem Cell ◽

Memory Acquisition ◽

Ad Therapy

In Alzheimer disease (AD) patients, degeneration of the cholinergic system utilizing acetylcholine for memory acquisition is observed. Since AD therapy using acetylcholinesterase (AChE) inhibitors are only palliative for memory deficits without slowing or reversing disease progress, there is a need for effective therapies, and stem cell-based therapeutic approaches targeting AD should fulfill this requirement. We established a human neural stem cell (NSC) line encoding choline acetyltransferase (ChAT) gene, an acetylcholine-synthesizing enzyme. APPswe/PS1dE9 AD model mice transplanted with the F3.ChAT NSCs exhibited improved cognitive function and physical activity. Transplanted F3.ChAT NSCs in the AD mice differentiated into neurons and astrocytes, produced ChAT protein, increased the ACh level, and improved the learning and memory function. F3.ChAT cell transplantation reduced Aβ deposits by recovering microglial function; i.e., the down-regulation of β-secretase and inflammatory cytokines and up-regulation of Aβ-degrading enzyme neprilysin. F3.ChAT cells restored growth factors (GFs) and neurotrophic factors (NFs), and they induced the proliferation of NSCs in the host brain. These findings indicate that NSCs overexpressing ChAT can ameliorate complex cognitive and physical deficits of AD animals by releasing ACh, reducing Aβ deposit, and promoting neuroregeneration by the production of GFs/NFs. It is suggested that NSCs overexpressing ChAT could be a candidate for cell therapy in advanced AD therapy.

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The Self-Fulfilling Prophecy of Episodic Memory Impairment in Mild Cognitive Impairment: Do Episodic Memory Deficits Identified at Classification Remain Evident When Later Examined with Different Memory Tests?

Neurology Research International ◽

10.1155/2013/437013 ◽

2013 ◽

Vol 2013 ◽

pp. 1-6 ◽

Cited By ~ 1

Author(s):

Shannon Zofia Klekociuk ◽

Mathew James Summers

Keyword(s):

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Episodic Memory ◽

Verbal Memory ◽

Memory Function ◽

Memory Deficits ◽

Memory Tests ◽

Amnestic Mci ◽

Screening Assessment ◽

Multiple Domain

Previous studies of mild cognitive impairment (MCI) have been criticised for using the same battery of neuropsychological tests during classification and longitudinal followup. The key concern is that there is a potential circularity when the same tests are used to identify MCI and then subsequently monitor change in function over time. The aim of the present study was to examine the evidence of this potential circularity problem. The present study assessed the memory function of 72 MCI participants and 50 healthy controls using an alternate battery of visual and verbal episodic memory tests 9 months following initial comprehensive screening assessment and MCI classification. Individuals who were classified as multiple-domain amnestic MCI (a-MCI+) at screening show a significantly reduced performance in visual and verbal memory function at followup using a completely different battery of valid and reliable tests. Consistent with their initial classification, those identified as nonamnestic MCI (na-MCI) or control at screening demonstrated the highest performance across the memory tasks. The results of the present study indicate that persistent memory deficits remain evident in amnestic MCI subgroups using alternate memory tests, suggesting that the concerns regarding potential circularity of logic may be overstated in MCI research.

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Long-Term Memory Deficits are Associated with Elevated Synaptic ERK1/2 Activation and Reversed by mGluR5 Antagonism in an Animal Model of Autism

Neuropsychopharmacology ◽

10.1038/npp.2014.13 ◽

2014 ◽

Vol 39 (7) ◽

pp. 1664-1673 ◽

Cited By ~ 38

Author(s):

Ronald R Seese ◽

Anna R Maske ◽

Gary Lynch ◽

Christine M Gall

Keyword(s):

Animal Model ◽

Memory Deficits ◽

Long Term Memory ◽

Term Memory

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Intrauterine growth restriction causes cellular, molecular, and behavioral deficits consistent with abnormal dentate gyrus neurogenesis in mice

10.1101/2020.07.16.207449 ◽

2020 ◽

Author(s):

Ashley S. Brown ◽

Matthew Wieben ◽

Shelby Murdock ◽

Jill Chang ◽

Maria Dizon ◽

...

Keyword(s):

Dentate Gyrus ◽

Learning And Memory ◽

Intrauterine Growth Restriction ◽

Memory Function ◽

Memory Deficits ◽

Growth Restriction ◽

Environmental Signals ◽

Intrauterine Growth ◽

Increased Risk ◽

Learning And Memory Deficits

AbstractBackgroundChildren born with intrauterine growth restriction (IUGR) are at increased risk for cognitive impairment including learning and memory deficits. Dentate gyrus (DG) granule neurons relay cortical information into the hippocampus proper for memory formation, and their production is highly dependent on environmental signals. However, it is unknown whether IUGR affects DG neurogenesis, and thus provides a potential mechanism underlying abnormal learning and memory function.MethodsUsing a hypertensive disease of pregnancy mouse model of IUGR, we assessed multiple behaviors, quantified neural stem and progenitor cells (NSPCs) and developing neurons in the DG, and characterized transcriptional effects on molecular pathways in the hippocampus.ResultsWe found that the predominant behavioral phenotype in IUGR offspring, short-term implicit learning and memory deficits, was associated with accelerated DG neurogenesis and NSPC depletion. Consistent with known molecular regulators of DG neurogenesis, we also found strong evidence for decreased Wnt pathway activity following IUGR.ConclusionWe have discovered that postnatal memory deficits are associated with accelerated NSPC differentiation following IUGR, a phenotype that could be explained by decreased Wnt signaling.

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Recollection memory deficits in patients with major depressive disorder predicted by past depressions but not current mood state or treatment status

Psychological Medicine ◽

10.1017/s0033291701004834 ◽

2002 ◽

Vol 32 (2) ◽

pp. 251-258 ◽

Cited By ~ 71

Author(s):

G. M. MacQUEEN ◽

T. M. GALWAY ◽

J. HAY ◽

L. T. YOUNG ◽

R. T. JOFFE

Keyword(s):

Medial Temporal Lobe ◽

Mood State ◽

Memory Performance ◽

Memory Function ◽

Memory Task ◽

Antidepressant Medication ◽

Memory Deficits ◽

Memory Systems ◽

Course Of Illness ◽

Current Mood

Background. Neuropsychological studies have suggested that memory systems reliant on medial temporal lobe structures are impaired in patients with depression. There is less data regarding whether this impairment is specific to recollection memory systems, and whether clinical features predict impairment. This study sought to address these issues.Method. A computerized process-dissociation memory task was utilized to dissociate recollection and habit memory in 40 patients with past or current major depression and 40 age, sex and IQ matched non-psychiatric control subjects. The Cognitive Failures Questionnaire was used to assess patients’ perceptions of day-to-day memory failures.Results. Patients had impaired recollection memory (t = 4·7, P<0·001), but no impairment in habit memory when compared to controls. Recollection memory performance was not predicted by indices of current mood state, but was predicted by self-assessments of impairment (β = −0·33; P = 0·008) and past number of depressions (β = −0·41; P = 0·001). There was no evidence that standard therapy with antidepressant medication either improved or worsened memory performance.Conclusions. The results confirm that patients with multiple past depressions have reduced function on recollection memory tasks, but not on habit memory performance. The memory deficits were independent of current mood state but related to past course of illness and significant enough that patients detected impairment in day-to-day memory function.

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Withdrawal from Extended, Intermittent Access to A Highly Palatable Diet Impairs Hippocampal Memory Function and Neurogenesis: Effects of Memantine

Nutrients ◽

10.3390/nu12051520 ◽

2020 ◽

Vol 12 (5) ◽

pp. 1520 ◽

Cited By ~ 2

Author(s):

Antonio Ferragud ◽

Clara Velázquez-Sánchez ◽

Ali Al Abdullatif ◽

Valentina Sabino ◽

Pietro Cottone

Keyword(s):

Memory Function ◽

Memory Deficits ◽

Chow Group ◽

Hippocampal Neurogenesis ◽

Palatable Food ◽

Hippocampal Function ◽

Proliferating Cells ◽

Intermittent Access ◽

Male Wistar Rats ◽

Palatable Diet

Background: Compulsive eating can be promoted by intermittent access to palatable food and is often accompanied by cognitive deficits and reduction in hippocampal plasticity. Here, we investigated the effects of intermittent access to palatable food on hippocampal function and neurogenesis. Methods: Male Wistar rats were either fed chow for 7 days/week (Chow/Chow group), or fed chow intermittently for 5 days/week followed by a palatable diet for 2 days/week (Chow/Palatable group). Hippocampal function and neurogenesis were assessed either during withdrawal or following renewed access to palatable food. Furthermore, the ability of the uncompetitive N-methyl-d-aspartate receptor (NMDAR) antagonist memantine to prevent the diet-induced memory deficits and block the maladaptive feeding was tested. Results: Palatable food withdrawn Chow/Palatable rats showed both a weakened ability for contextual spatial processing and a bias in their preference for a “novel cue” over a “novel place,” compared to controls. They also showed reduced expression of immature neurons in the dentate gyrus of the hippocampus as well as a withdrawal-dependent decrease of proliferating cells. Memantine treatment was able both to reverse the memory deficits and to reduce the excessive intake of palatable diet and the withdrawal-induced hypophagia in food cycling rats. Conclusions: In summary, our results provide evidence that withdrawal from highly palatable food produces NMDAR-dependent deficits in hippocampal function and a reduction in hippocampal neurogenesis.

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S207. CHRONIC TREATMENT WITH 1METIQ INDUCES PRO-COGNITIVE EFFECT ON RECOGNITION MEMORY IN KETAMINE MODEL OF SCHIZOPHRENIA IN RATS

Schizophrenia Bulletin ◽

10.1093/schbul/sbaa031.273 ◽

2020 ◽

Vol 46 (Supplement_1) ◽

pp. S117-S117

Author(s):

Magdalena Białoń ◽

Agnieszka Wąsik ◽

Marcelina Żarnowska

Keyword(s):

Recognition Memory ◽

Glutamate Release ◽

Statistical Significance ◽

Memory Function ◽

Memory Deficits ◽

Mammalian Brain ◽

Control Group ◽

World Population ◽

Sprague Dawley ◽

Cognitive Effect

Abstract Background Schizophrenia is severe mental disorder that affects 1% of world population and cause long-term disability (Mueser and McGurk, 2004). Manifestation of the illness can be distinguished into three groups – positive, negative and cognitive symptoms (van Os, 2009). However, cognitive ones (e.g. memory deficits) seem to remain resistant to pharmacotherapy (Cerveri et al., 2019). Memory deficits, as a symptoms of schizophrenia, may be modeled in animals by using a specified dose of ketamine and measured in novel object recognition (NOR) test (Lafionatis et al., 2019). 1-methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) is an endogenous amine present and synthesized in the mammalian brain with neuroprotective properties (Antkiewicz-Michaluk et al., 2014) and our last study have shown anxiolytic action of 1MeTIQ in rat model of schizophrenia (Wąsik et al., 2019) therefore we decided to define a potential of 1MeTIQ to exhibit pro-cognitive effect on memory in ketamine-treated rats. Methods NOR test consisted of adaptation (24h before testing) and two phases (T1 and T2, with 1-hour interval). Exploration times of each objects, preference (PI) and discrimination (DI) indexes were measured. Microdialysis was performed to asses glutamate release in frontal cortex. Male Sprague Dawley rats were divided into 4 groups. The control group received saline injections. Animals received acute ketamine (20mg/kg, i.p.) or chronic (7x) administration of1MeTIQ (50mg/kg, i.p.). The combined group received single dose of ketamine 30 minutes after last dose of 1MeTIQ. Results In T1 phase of NOR, there were no changes between exploration times of two identical objects. In T2 phase with two different objects, we observed no significant changes in group treated with ketamine. 1MeTIQ given alone increased the difference between time of objects exploration. In combined group, 1MeTIQ completely reversed the effect of ketamine. Ketamine tended, however, without statistical significance, to decrease PI and DI. Treatment with 1MeTIQ did not change mentioned indexes. In microdialysis study, we observed no significant changes in glutamate release in any group. Discussion We demonstrated that chronic administration of 1MeTIQ may improve recognition memory function. However, we didn’t observe changes in glutamate release. We suggest that pro-cognitive effect of 1MeTIQ is associated with its impact on monoamine metabolism.

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