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)

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.
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PMID:The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures. 1462 99

Alzheimer's disease (AD) characteristically presents with early memory loss. Regulation of K(+) channels, calcium homeostasis, and protein kinase C (PKC) activation are molecular events that have been implicated during associative memory which are also altered or defective in AD. PKC is also involved in the processing of the amyloid precursor protein (APP), a central element in AD pathophysiology. In previous studies, we demonstrated that benzolactam (BL), a novel PKC activator, reversed K(+) channels defects and enhanced secretion of APP alpha in AD cells. In this study we present data showing that another PKC activator, bryostatin 1, at subnanomolar concentrations dramatically enhances the secretion of the alpha-secretase product sAPP alpha in fibroblasts from AD patients. We also show that BL significantly increased the amount of sAPP alpha and reduced A beta 40 in the brains of APP[V717I] transgenic mice. In a more recently developed AD double-transgenic mouse, bryostatin was effective in reducing both brain A beta 40 and A beta 42. In addition, bryostatin ameliorated the rate of premature death and improved behavioral outcomes. Collectively, these data corroborate PKC and its activation as a potentially important means of ameliorating AD pathophysiology and perhaps cognitive impairment, thus offering a promising target for drug development. Because bryostatin 1 is devoid of tumor-promoting activity and is undergoing numerous clinical studies for cancer treatment in humans, it might be readily tested in patients as a potential therapeutic agent for Alzheimer's disease.
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PMID:Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice. 1526 77

Limbic encephalitis was identified as a clinicopathological entity in 1968. Up to a few years ago, 200 cases were described, most associated with lung cancer and more infrequently with other tumors. The recent identification of patients with this syndrome, idiopathic limbic encephalitis, who never develop cancer and have high titers of antibodies to voltage-gated potassium channels (VGKC) and an excellent response to immunosuppressive therapy, has extended the etiological spectrum and suggests that the syndrome may be under-recognized. The disorder, which develops in a few days or weeks, is characterized by the development of short-term memory loss, seizures, confusion and psychiatric features. The presence of symptoms beyond the limbic system is highly suggestive of a paraneoplastic origin. When limbic encephalitis is suspected, the following tests should be performed in order to demonstrate: a) involvement of the temporal lobes (EEG and brain MRI); b) presence of inflammatory abnormalities in the CSF, and c) the presence of onconeural antibodies or anti-VGKC. Once the diagnosis is confirmed by the clinical picture and MRI findings, treatment must be initiated without waiting for the antibody results because its negativity does not exclude the diagnosis. Detection of an onconeural antibody will confirm that the limbic syndrome is paraneoplastic and will help us to search for an underlying tumor and to predict possible response to the treatment. The recommended treatment is cycles of methylprednisolone (1 g/day for 3 to 5 days). Therapeutic response in the idiopathic limbic encephalitis is excellent and may be good in limbic encephalitis with anti-Ma2 or without onconeural antibodies. On the contrary, immunosuppressant treatment is not usually effective in limbic encephalitis associated to anti-Hu antibodies.
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PMID:[Limbic encephalitis: a probably under-recognized syndrome]. 1570 18

The paper describes the case of a 49 year old woman suffering from bipolar affective disorder, who additionally had a brain xanthogranuloma tumour. The symptoms that occurred additionally to affective disorder symptoms were loss of memory, with some events forgotten completely, vertigo and deteriorated visual accommodation. The ophthalmology examination could not explain the worsening accommodation. It turned out that a brain tumour was the cause of these symptoms and they all receded after the tumour's total resection. This kind of tumour--a xanthogranuloma is a rare pseudoneoplasm, very often pretending to be a cancer in various body organs. It happens to be very rare in the above mentioned isolated form in the brain and until now, only a few cases have been described as diagnosed in a live person.
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PMID:[A case of brain xanthogranuloma, that developed during bipolar affective disorder]. 1577 Nov 55

Primary indolent leptomeningeal lymphoma is a rare entity, and corresponds in most cases to mucosa-associated lymphoid tissue (MALT) type lymphoma. We are reporting a case of a 75 years old woman, who presented with a 2-year history of behavioral disorder, progressive memory loss and aphasia. Neuroimaging showed a mass infiltrating the frontal circumvolutions and the roof of the orbit. The biopsy revealed an infiltration of the dura by an indolent lymphoma, characteristic of a MALT-type lymphoma. Complete staging work-up did not show any evidence of systemic involvement. A treatment with systemic methotrexate, combined with intrathecal chemotherapy and followed by radiotherapy (30,6 Gy) of the primary site, was conducted. The 3-year follow-up confirms the persistent remission, the patient remaining well and free of symptoms. The review of the literature highlights the importance to recognize the indolent PLML as a distinct clinical entity, which exhibits a rather good prognosis following a relatively non-toxic therapy.
Bull Cancer 2005 Jul
PMID:Primary intracranial dural lymphoma of mucosa-associated lymphoid tissue (MALT) type: report of one case and review of the literature. 1612 99

Memory loss can be a symptom of paraneoplastic limbic encephalitis (PLE) a neuropsychiatric disorder associated mostly with small-cell lung cancer and anti-Hu antibodies or with testicular tumors and anti-Ma2 antibodies. We present the case of a patient with temporal coincidence of beginning cognitive decline and diagnosis of a carcinoma of the prostate in whom we diagnosed anti-Ma1/Ma2-positive PLE. The tumor had been completely resected but memory impairment further deteriorated. As the effective treatment of the cancer is considered as the most efficient treatment of a paraneoplastic neurological syndrome (PNS) a second neoplasia was suspected in the patient. By the aid of whole body positron emission tomography with 18-fluorine fluoro-2-deoxy-glucose (FDG-PET) an adenocarcinoma of the cecum could be detected. Two months after surgery anti-Ma antibodies were negative. We conclude that a second neoplasia should be considered, if effective cancer treatment does not lead to improvement or stabilisation of a PNS. Tumor search should be exhaustive and include PET when conventional imaging fails to show a malignancy.
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PMID:Second primary tumor in anti-Ma1/2-positive paraneoplastic limbic encephalitis. 1631 42

Several types of mass lesions may occur in the third and lateral ventricles. Typically they arise from the lining of the ventricular cavity or from contiguous structures, by extension into the ventricle. The authors describe two patients, each of whom presented with a different rare lesion of the ventricular system. The first was a 53-year-old woman with a history of hypertension who sustained a blunt traumatic injury to the occipital region and subsequently developed a progressively worsening right-sided headache. Radiological examinations over the next 2 years revealed an enlarged right lateral ventricle and, ultimately, a choroid plexus cyst in its anterior and middle third, near the foramen of Monro, which is a rare location for these lesions. The cyst was removed en bloc, and follow-up examinations showed a significant improvement in her headache and a minimal differences in size between right and left ventricles. The authors also describe a 57-year-old man with hypertension, diabetes mellitus, and an old mycardial infarct, who presented to an outside institution with a progressively worsening headache, generalized malaise, and loss of olfactory sensation. Diagnostic imaging revealed a 1.5-cm oval lesion centered in the lamina terminalis region, an open craniotomy was performed, and evaluation of a biopsy sample demonstrated the mass to be a chordoid glioma of the third ventricle, a recently described glioma subtype. Two days after surgery, he suffered a left parietal stroke and an anterior mycardial infarction. After convalescing, he presented to The University of Texas M. D. Anderson Cancer Center for radiotherapy and follow up; 7 months later he was readmitted complaining of headache, short-term memory loss, and worsening confusion and disorientation. Neuroimaging revealed progression of the tumor (now 2 cm in diameter), which was removed by gross-total resection. His headache resolved immediately, and 2 months later his only complaint was of episodes of confusion. Three weeks later he died of a massive myocardial infarction. These two patients represent the sixth case of an adult with a choroid plexus cyst in the anterior lateral ventricle and the 19th case of an adult with a chordoid glioma of the third ventricle, respectively.
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PMID:Choroid plexus cyst and chordoid glioma. Report of two cases. 1672 23

The development of novel chemotherapeutic agents and advances in treatment technique have improved survival for patients diagnosed with some forms of cancer, but treatments are not always site specific and may place normal tissues at risk. The central nervous system (CNS) is susceptible to treatment effects and complaints of memory loss and generalized cognitive decline are common among cancer patients. Despite the frequency of subjective patient complaints, studies evaluating the cognitive abilities of patients have inconsistently reported chemotherapy-related declines. On careful review of the literature, discrepant findings across studies (some documenting chemotherapy-related cognitive declines and others failing to detect such changes) may be attributed to differences in methodology. Most studies have been retrospective in design, omit pretreatment assessment of function, use small or heterogeneous samples, use inappropriate measures to assess cognition, and fail to incorporate control subjects. Though rare to date, prospective, randomized, longitudinal studies that incorporate pretreatment comprehensive neuropsychological assessment are necessary to define the severity and pattern of treatment-related change. Building on a foundation of solid science, future studies may identify subgroups of patients susceptible to significant chemotherapy-related cognitive decline. Once these groups are identified and the mechanisms underlying the decline are elucidated, attention may be turned to the development of treatments that may optimize cognitive function and improve patient quality of life.
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PMID:Chemotherapy and cognition: effects, potential mechanisms, and management. 1685 72

The aim of this paper is to briefly describe the unique methodology employed by nine nurse researchers who conducted research into the social and emotional effects of chemotherapy from the patient's perspective, and to present four dominant themes. The research developed from discussions at a local UK Nurses Oncology Forum, during which nurses voiced their concern about the social and emotional implications for people receiving chemotherapy. It was anticipated that understanding the issues from the patient's perspective would assist nurses to reconsider and reshape the care provided, particularly in the chemotherapy clinic. Using principles of phenomenology, the nurse researchers collected data from participants using conversational-style interviews. Some participants kept diaries of chemotherapy experiences. These data were subsequently analysed using a modified phenomenological analysis framework. Nineteen people were recruited to the study, resulting in 98 interviews and seven diaries. Eight major themes emerged from the data: striving for normality, the role of significant others, feeling up - feeling down, flagging, being sociable, anxiety, the chemotherapy process, and participating in the research. Relationship dynamics, the perceived role of significant others and the frustrations associated with lack of concentration and memory loss are important findings that should influence nursing care and management.
Eur J Cancer Care (Engl) 2007 Jan
PMID:The social and emotional toll of chemotherapy - patients' perspectives. 1722 52

Adriamycin (ADR), a potent anti-tumor agent, produces reactive oxygen species (ROS) in cardiac tissue. Treatment with ADR is dose-limited by cardiotoxicity. However, the effect of ADR in the other tissues, including the brain, is unclear because ADR does not pass the blood-brain barrier. Some cancer patients receiving ADR treatment develop a transient memory loss, inability to handle complex tasks etc., often referred to by patients as chemobrain. We previously demonstrated that ADR causes CNS toxicity, in part, via systemic release of cytokines and subsequent generation of reactive oxygen and nitrogen species (RONS) in the brain. Here, we demonstrate that treatment with ADR led to an increased circulating level of tumor necrosis factor-alpha in wild-type mice and in mice deficient in the inducible form of nitric oxide (iNOSKO). However, the decline in mitochondrial respiration and mitochondrial protein nitration after ADR treatment was observed only in wild-type mice, not in the iNOSKO mice. Importantly, the activity of a major mitochondrial antioxidant enzyme, manganese superoxide dismutase (MnSOD), was reduced and the protein was nitrated. Together, these results suggest that NO is an important mediator, coupling the effect of ADR with cytokine production and subsequent activation of iNOS expression. We also identified the mitochondrion as an important target of ADR-induced NO-mediated CNS injury.
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PMID:Adriamycin-mediated nitration of manganese superoxide dismutase in the central nervous system: insight into the mechanism of chemobrain. 1722 39


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