Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ameliorating effects of methanol extracts of Basidiomycetes against in vitro and in vivo model of Alzheimer's disease were investigated. The extracts of Cordyceps ophioglossoides and Hypocrea citrina var. citrina prevented the beta-amyloid((25-35)) (Abeta((25-35)))-induced cell death in SK-N-SH neuronal cells. However, in rat model of Alzheimer's disease, 30-d intraperitoneal administration with only the extract of Cordyceps ophioglossoides significantly prevented spatial memory loss by intracranial injection of Abeta((25-35)), which was assessed in water maze task. Interestingly, the scavenging activity of the reactive oxygen species (ROS) generated in Abeta((25-35))-treated cells was also found in the extract of Cordyceps ophioglossoides, but not in the extract of Hypocrea citrina var. citrina. These results suggest that the extract of Cordyceps ophioglossoides may protect the Abeta-induced neuronal cell death and memory loss through free radical scavenging activity. These results further suggest that Cordyceps ophioglossoides mycelium may be valuable for the protection from Alzheimer's dementia.
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PMID:Mycelial extract of Cordyceps ophioglossoides prevents neuronal cell death and ameliorates beta-amyloid peptide-induced memory deficits in rats. 1525 53

We have demonstrated that oxidative stress is involved, at least in part, in beta-amyloid protein (Abeta)-induced neurotoxicity in vivo [Eur. J. Neurosci. 1999;11:83-90; Neuroscience 2003;119:399-419]. However, mechanistic links between oxidative stress and memory loss in response to Abeta remain elusive. In the present study, we examined whether oxidative stress contributes to the memory deficits induced by intracerebroventricular injection of Abeta (1-42) in mice. Abeta (1-42)-induced memory impairments were observed, as measured by the water maze and passive avoidance tests, although these impairments were not found in Abeta (40-1)-treated mice. Treatment with antioxidant alpha-tocopherol significantly prevented memory impairment induced by Abeta (1-42). Increased activities of the cytosolic Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and mitochondrial Mn-superoxide dismutase (Mn-SOD) were observed in the hippocampus and cerebral cortex of Abeta (1-42)-treated animals, as compared with Abeta (40-1)-treated mice. The induction of Cu,Zn-SOD was more pronounced than that of Mn-SOD after Abeta (1-42) insult. However, the concomitant induction of glutathione peroxidase (GPX) in response to significant increases in SOD activity was not seen in animals treated with Abeta (1-42). Furthermore, glutathione reductase (GRX) activity was only increased at 2h after Abeta (1-42) injection. Production of malondialdehyde (lipid peroxidation) and protein carbonyl (protein oxidation) remained elevated at 10 days post-Abeta (1-42), but the antioxidant alpha-tocopherol significantly prevented these oxidative stresses. Therefore, our results suggest that the oxidative stress contributes to the Abeta (1-42)-induced learning and memory deficits in mice.
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PMID:Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex. 1536 77

Whether high-cholesterol diets (HCD) induce a high incidence of memory deficits in diabetes requires to be established; if so, whether they induce impairments of memory acquired in the pre-diabetic stage as well as in the diabetic stage also needs to be elucidated, and part of the related mechanisms involved in this dysfunction should be determined. The mice were grouped into: normal mice fed normal diets (NN), diabetic mice fed normal diets (DN), normal mice fed HCD (NH), and diabetic mice fed HCD (DH). Animals were subjected to Morris water maze testing: 1) Learning in the pre-diabetic stage and memory retrieval in the diabetic stage; 2) Learning and memory retrieval in the diabetic stage. Following water maze testing, biochemical parameters were estimated in the animals. The results showed that significant impairments of memory retrieval, acquired in the diabetic stage, were observed only in DH group, neither in DN nor NH group in a short term compared with NN group. Biochemical parameters including fasting blood glucose, lipid peroxidation productions and acetylcholinesterase activities in frontal cortex and hippocampus increased more rapidly in DH group than those in the rest. These results indicate that HCD impair the diabetic retention of memory, but neither the diabetic acquisition of memory nor the pre-diabetic retention of memory in diabetic mice in a short term. Controlled HCD may be a strategy to prevent the loss of memory in diabetic individuals after they have acquired new information.
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PMID:High-cholesterol diets impair short-term retention of memory in alloxan-induced diabetic mice, but not acquisition of memory nor retention of memory in prediabetic mice. 1590 67

A 42-year-old Chinese woman presented with transient confusional state and memory loss due to acute water intoxicational hyponatremia complicating colonic irrigation (enemas) used as an alternative medicine to promote health. Although there is no evidence that such "antiautointoxication" technique conveys true benefit in any condition, this form of "quackery" may actually cause harm, such as water intoxication as in this case.
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PMID:Colonic irrigation-induced hyponatremia. 1632 64

Major depression is a mood disorder characterized by a sense of inadequacy, despondency, decreased activity, pessimism, anhedonia and sadness where these symptoms severely disrupt and adversely affect the person's life, sometimes to such an extent that suicide is attempted or results. Antidepressant drugs are not always effective and some have been accused of causing an increased number of suicides particularly in young people. Magnesium deficiency is well known to produce neuropathologies. Only 16% of the magnesium found in whole wheat remains in refined flour, and magnesium has been removed from most drinking water supplies, setting a stage for human magnesium deficiency. Magnesium ions regulate calcium ion flow in neuronal calcium channels, helping to regulate neuronal nitric oxide production. In magnesium deficiency, neuronal requirements for magnesium may not be met, causing neuronal damage which could manifest as depression. Magnesium treatment is hypothesized to be effective in treating major depression resulting from intraneuronal magnesium deficits. These magnesium ion neuronal deficits may be induced by stress hormones, excessive dietary calcium as well as dietary deficiencies of magnesium. Case histories are presented showing rapid recovery (less than 7 days) from major depression using 125-300 mg of magnesium (as glycinate and taurinate) with each meal and at bedtime. Magnesium was found usually effective for treatment of depression in general use. Related and accompanying mental illnesses in these case histories including traumatic brain injury, headache, suicidal ideation, anxiety, irritability, insomnia, postpartum depression, cocaine, alcohol and tobacco abuse, hypersensitivity to calcium, short-term memory loss and IQ loss were also benefited. Dietary deficiencies of magnesium, coupled with excess calcium and stress may cause many cases of other related symptoms including agitation, anxiety, irritability, confusion, asthenia, sleeplessness, headache, delirium, hallucinations and hyperexcitability, with each of these having been previously documented. The possibility that magnesium deficiency is the cause of most major depression and related mental health problems including IQ loss and addiction is enormously important to public health and is recommended for immediate further study. Fortifying refined grain and drinking water with biologically available magnesium to pre-twentieth century levels is recommended.
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PMID:Rapid recovery from major depression using magnesium treatment. 1654 86

Mutations in presenilins (PS) 1 and 2 are the major cause of familial Alzheimer's disease. Conditional inactivation of PS1 in the mouse postnatal forebrain leads to mild deficits in spatial learning and memory, whereas inactivation of both PS1 and PS2 results in severe memory and synaptic plasticity impairments, followed by progressive and substantial neurodegeneration. Here we investigate the effect of a familial Alzheimer's disease-linked PS1 missense mutation using knock-in (KI) mice, in which the wild-type PS1 allele is replaced with the M146V mutant allele. In the Morris water maze task, PS1 KI mice at 3 months of age exhibit reduced quadrant occupancy and platform crossing in the probe trial after 6 days of training, though their performance was normal in the probe trial after 12 days of training. By the age of 9 months, even after 12 days of training, PS1 homozygous KI mice still exhibit reduced platform crossing in the post-training probe trial. ELISA analysis revealed a selective increase in cortical levels of beta-amyloid 42 in PS1 KI mice, whereas production of beta-amyloid 40 was normal. Histological and quantitative real-time RT-PCR analyses showed normal gross hippocampal morphology and unaltered expression of three genes involved in inflammatory responses in PS1 KI mice. These results show hippocampal spatial memory impairments caused by the PS1 M146V mutation and age-related deterioration of the memory impairment, suggesting that PS1 KI mice are a valuable model system for the study of memory loss in AD.
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PMID:Hippocampal spatial memory impairments caused by the familial Alzheimer's disease-linked presenilin 1 M146V mutation. 1690 98

The manner in which hormone therapy is given to postmenopausal women may significantly influence its ability to reduce age-associated memory loss. To test the hypothesis that a regimen that approximates the timing of estrogen surges in the natural cycle is more beneficial for memory than a regimen that provides continuous levels of estrogen, we examined the effects of continuous and intermittent estrogen regimens on spatial and object memory in aging female mice. Mice (18 months) were treated with 0.2 mg/kg 17beta-estradiol (E(2)) or vehicle (VEH) for 3 months following ovariectomy. A fast-acting water-soluble cyclodextrin-encapsulated E(2) was used to ensure metabolism within 24 h. Vehicle-treated mice received daily injections of 2-hydroxypropyl-beta-cyclodextrin vehicle. The continuous estradiol group (Contin E(2)) was injected daily with estradiol. The intermittent group (Twice/wk E(2)) received estradiol every 4 days and vehicle on all other days. Mice (21 months) were tested in water-escape motivated 8-arm radial arm maze (WRAM) and object recognition tasks. During WRAM acquisition, the Twice/wk E(2) group committed significantly more reference memory errors than VEH and Contin E(2) groups, and tended to make more working memory errors than the VEH group. The Contin E(2) group did not differ from VEH on either WRAM measure. Additionally, the Twice/wk E(2) group tended to exhibit impaired object recognition. Thus, neither treatment improved spatial or object memory. Indeed, intermittent estradiol was detrimental to both types of memory. These results suggest that the timing of administration may play an important role in the mnemonic response of aging females to estrogen.
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PMID:Effects of continuous and intermittent estrogen treatments on memory in aging female mice. 1692 82

Angiotensin converting enzyme inhibitors (ACEis) are widely used anti-hypertensive agents that are also reported to have positive effects on mood and cognition. The present study examined the influence of the ACEi, perindopril, on cognitive performance and anxiety measures in rats. Two groups of rats were treated orally for one week with the ACEi, perindopril, at doses of 0.1 and 1.0mg/kg/day. Learning was assessed by the reference memory task in the water maze, comparing treated to control rats. Over five training days both perindopril-treated groups learnt the location of the submerged platform in the water maze task significantly faster than control rats. A 60s probe trial on day 6 showed that the 1.0mg/kg/day group spent significantly longer time in the training quadrant than control rats. This improved performance in the swim maze task was not due to the effect of perindopril on motor activity or the anxiety levels of the rats as perindopril-treated and control animals behaved similarly in activity boxes and on the elevated+maze. These results confirm the anecdotal human studies that ACEis have a positive influence on cognition and provide possibilities for ACEis to be developed into therapies for memory loss.
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PMID:Effect of chronic angiotensin converting enzyme inhibition on spatial memory and anxiety-like behaviours in rats. 1701 2

Exposure to fungi, particularly in water damaged indoor environments, has been thought to exacerbate a number of adverse health effects, ranging from subjective symptoms such as fatigue, cognitive difficulties or memory loss to more definable diseases such as allergy, asthma and hypersensitivity pneumonitis. Understanding the role of fungal exposure in these environments has been limited by methodological difficulties in enumerating and identifying various fungal components in environmental samples. Consequently, data on personal exposure and sensitization to fungal allergens are mainly based on the assessment of a few select and easily identifiable species. The contribution of other airborne spores, hyphae and fungal fragments to exposure and allergic sensitization are poorly characterized. There is increased interest in the role of aerosolized fungal fragments following reports that the combination of hyphal fragments and spore counts improved the association with asthma severity. These fragments are particles derived from any intracellular or extracellular fungal structure and are categorized as either submicron particles or larger fungal fragments. In vitro studies have shown that submicron particles of several fungal species are aerosolized in much higher concentrations (300-500 times) than spores, and that respiratory deposition models suggest that such fragments of Stachybotrys chartarum may be deposited in 230-250 fold higher numbers than spores. The practical implications of these models are yet to be clarified for human exposure assessments and clinical disease. We have developed innovative immunodetection techniques to determine the extent to which larger fungal fragments, including hyphae and fractured conidia, function as aeroallergen sources. These techniques were based on the Halogen Immunoassay (HIA), an immunostaining technique that detects antigens associated with individual airborne particles >1 microm, with human serum immunoglobulin E (IgE). Our studies demonstrated that the numbers of total airborne hyphae were often significantly higher in concentration than conidia of individual allergenic genera. Approximately 25% of all hyphal fragments expressed detectable allergen and the resultant localization of IgE immunostaining was heterogeneous among the hyphae. Furthermore, conidia of ten genera that were previously uncharacterized could be identified as sources of allergens. These findings highlight the contribution of larger fungal fragments as aeroallergen sources and present a new paradigm of fungal exposure. Direct evidence of the associations between fungal fragments and building-related disease is lacking and in order to gain a better understanding, it will be necessary to develop diagnostic reagents and detection methods, particularly for submicron particles. Assays using monoclonal antibodies enable the measurement of individual antigens but interpretation can be confounded by cross-reactivity between fungal species. The recent development of species-specific monoclonal antibodies, used in combination with a fluorescent-confocal HIA technique should, for the first time, enable the speciation of morphologically indiscernible fungal fragments. The application of this novel method will help to characterize the contribution of fungal fragments to adverse health effects due to fungi and provide patient-specific exposure and sensitization profiles.
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PMID:Airborne fungal fragments and allergenicity. 1705 Apr 46

Temporal lobe epilepsy is characterized by a progressive loss of memory capacities, due to sclerosis and functional impairment of mesiotemporal brain areas. We have shown recently that topiramate (TPM) dose-dependently protects hippocampal CA1 and CA3 neurons during initial status epilepticus in the rat pilocarpine model of temporal lobe epilepsy by inhibition of mitochondrial transition pore opening. In the present study, in order to evaluate possible positive effects of the treatment on learning and memory, we investigated water maze performance of rats receiving different dosages of TPM (20 and 100 mg/kg) after 40 min and 4 mg/kg diazepam after 160 min of pilocarpine-induced status epilepticus in relation to performance of animals receiving 4 mg/kg diazepam after 40 min of SE, and to performance of sham-treated control animals. Unexpectedly, 20 but not 100 mg/kg TPM significantly extenuated short-term memory deficits. While neuroprotective effects of TPM were observed in hippocampal CA subfields of animals treated with 100 mg/kg TPM, cell loss in rats treated with 20 mg/kg TPM was indistinguishable from animals receiving diazepam only. The present results indicate a negative dose-dependency of memory-saving effects of TPM applied during status epilepticus apparently dissociated from hippocampal neuroprotection.
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PMID:Amelioration of water maze performance deficits by topiramate applied during pilocarpine-induced status epilepticus is negatively dose-dependent. 1708 66


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