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)

The presence of insulin receptor in the hippocampus suggests that this organ is a target for insulin. However, unlike the classic peripheral insulin target tissues such as adipocyte, muscle and liver, where the primary function of insulin is to regulate glucose homeostasis, insulin in the central nervous system (CNS) exhibits more diverse actions, most of which have not been clearly understood. A direct role of hippocampal insulin receptor signaling in improving cognitive functions, including learning and memory, and the association of insulin receptor deterioration with brain degenerative dementia (e.g., Alzheimer's disease) have attracted increasing interest. Additionally it has been shown that insulin can be a neuroprotective agent against memory loss induced by ischemia, lesions and some pharmacological agents. In the present study we evaluate the hypothesis that the bilateral intra CA1 insulin injection can protects against stress-induced memory deficit. Chronic restraint stress (2h per day x 7 days) significantly impaired spatial performance in Morris water maze and elevated serum corticosterone level. Intrahippocampal insulin microinjection was done 15-20 min before every stress episode. Insulin in low dose (0.5 MU) had no significant effect on memory deficit induced by stress. But in higher doses (6 and 12 MU) insulin protects animals against the deleterious effect of stress. Insulin alone daily injection had no effect on water maze performance. These results suggest that spatial learning and memory is compromised during chronic stress and insulin may protect against this effect.
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PMID:Insulin protects against stress-induced impairments in water maze performance. 1711 37

Studies involving animal models of acute central nervous system (CNS) stroke and trauma strongly indicate that sex and/or hormonal status are important determinants of outcome after brain injury. The present study was undertaken to examine the ability of estradiol to protect hippocampal neurons from lateral fluid percussion brain injury. Sprague-Dawley female rats (211-285 g; n = 119) were ovariectomized, and a subset (n = 66) were implanted with 17beta-estradiol pellets to provide near physiological levels of estradiol. Animals were subjected to lateral fluid percussion brain injury or sham injury 1 week later. Activation of caspase-3 (n = 26) and TUNEL staining (n = 21) were assessed at 3 and 12 h after injury, respectively, in surviving control and estradiol-treated animals. Memory retention was examined using a Morris water maze test in a separate subset of animals (n = 43) at 8 days after injury. Activated caspase-3 and TUNEL staining were observed in the dentate hilus, granule cell layer, and CA3 regions in all injured rats, indicative of selective hippocampal cell apoptosis in the acute posttraumatic period. Estradiol did not significantly alter the number of hippocampal neurons exhibiting caspase-3 activity or TUNEL staining. Brain injury impaired cognitive ability, assessed at 1 week post-injury (p < 0.001). However, estradiol at physiological levels did not significantly alter injury-induced loss of memory. These data indicate that estradiol at physiological levels does not ameliorate trauma-induced hippocampal injury or cognitive deficits in ovariectomized female rats.
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PMID:Effects of estradiol on cognition and hippocampal pathology after lateral fluid percussion brain injury in female rats. 1718 91

The fast ripening of fruits means they may contain various harmful properties. A commonly used agent in the ripening process is calcium carbide, a material most commonly used for welding purposes. Calcium carbide treatment of food is extremely hazardous because it contains traces of arsenic and phosphorous. Once dissolved in water, the carbide produces acetylene gas. Acetylene gas may affect the neurological system by inducing prolonged hypoxia. The findings are headache, dizziness, mood disturbances, sleepiness, mental confusion, memory loss, cerebral edema and seizures. We report the case of a previously healthy 5 year-old girl with no chronic disease history who was transferred to our Emergency Department with an 8-h history of coma and delirium. A careful history from her father revealed that the patient ate unripe dates treated with calcium carbide.
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PMID:Calcium carbide poisoning via food in childhood. 1730 29

The achiral sodium salt of poly(4-carboxyphenyl isocyanide) (poly-1-Na) folds into a one-handed helix induced by optically active amines in water. The induced helicity remains when the optically active amines are completely removed, and further modification of the side groups to amide residues is possible without loss of memory of macromolecular helicity. Although the helical poly-1-Na loses its chiral memory at high temperature, helical polyisocyanides modified with achiral primary amines, which no longer have any chiral components, keep their memory perfectly even at 100 degrees C in N,N-dimethylformamide in some cases and exhibit cholesteric liquid-crystalline phases, thus providing a robust scaffold with heat resistance to which a variety of functional groups can be introduced.
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PMID:Unexpected thermally stable, cholesteric liquid-crystalline helical polyisocyanides with memory of macromolecular helicity. 1745 38

Short and long term memory loss may result from deteriorating cerebral mechanisms due to varied causes which could have a tremendous impact on the quality of life. Herbs are being constantly explored to resolve cognitive deficits. Eclipta alba (Ea) commonly called as the trailing Eclipta is being examined for its memory enhancing quality as it is traditionally used for this purpose. The shade dried leaves of Eclipta alba was extracted with distilled water. The suspension of Ea containing 100 and 200 mg/kg was administered to rats to evaluate Transfer Latency (TL) on an elevated plus maze. TL was a measure of acquisition and retrieval learning. Mice were placed at the center of open field apparatus to assess spatial habitual learning, observed for 20 minutes for rearing and time spent during rearing using varied doses for 30 minutes, 24 hours and 96 hours and 144 hrs. The results revealed significant improvement of retrieval memory.
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PMID:Investigation on the effect of eclipta alba on animal models of learning and memory. 1834 Dec 24

The present study has been designed to pharmacologically investigate the role of mast cell degranulation in ischemic preconditioning-induced reversal of global ischemia- and reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion of 17 min followed by reperfusion for 24 h was employed in present study to produce ischemia- and reperfusion-induced cerebral injury in mice. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Memory was evaluated using Morris water-maze test. Rota-rod test was employed to assess motor incoordination. Bilateral carotid artery occlusion followed by reperfusion produced cerebral infarction and impaired memory and motor coordination. Three preceding episodes of bilateral carotid artery occlusion for 1 min and reperfusion of 1 min (ischemic preconditioning) prevented markedly ischemia-reperfusion-induced cerebral injury measured in terms of infarct size, loss of memory and motor coordination. Sodium cromoglycate (10 mg/kg, i.p.), a mast cell stabilizer attenuated the neuroprotective effect of ischemic preconditioning. It is concluded that neuroprotective effect of ischemic preconditioning may be due to the degranulation of mast cells.
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PMID:Implication of mast cell degranulation in ischemic preconditioning-induced prevention of cerebral injury. 1835 13

A consistent finding in patients suffering from Alzheimer's disease is a loss of the cholinergic neurons of the basal forebrain that project to the hippocampus. However, the role this depletion plays in the development of Alzheimer's disease remains unclear. The loss of this ascending neurotransmitter system could potentially render hippocampal neurons more susceptible to further insult, such as chronic stress, ultimately resulting in neuronal death and memory loss. We explored this possibility by using the highly specific toxin 192 IgG-Saporin to destroy the majority of cholinergic activity in the septo-hippocampal pathway in rats. Following depletion, rats were subjected to 2 weeks of restraint stress. Rats were divided into two groups and were tested either on a hippocampal-dependent (water maze) task or a hippocampal-independent task (fear conditioning to tone and context). We showed that cholinergic depletion or stress alone had no effect on the successful performance of either of the tasks. However, rats with a combination of cholinergic depletion and stress were significantly impaired on the water-maze task. No deficits were apparent in the combined group that was tested on fear conditioning to tone or context, suggesting that this impairment is specific to spatial working memory. These rats had no obvious hippocampal neuronal loss or damage; however, there were likely subtle changes in hippocampal processing that led to the observed deficit on the hippocampal-dependent task. These findings support our theory that cholinergic depletion of the medial septum increases hippocampal vulnerability to further insults such as stress.
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PMID:Emergence of spatial impairment in rats following specific cholinergic depletion of the medial septum combined with chronic stress. 1844 17

Alzheimer's disease (AD) is the most common form of dementia in the elderly. Classic symptoms of the disease include memory loss and confusion associated with the hallmark neuro-pathologic lesions of neurofibrillary tangles (NFT) and senile plaques (SP) and their sequelae, gray matter atrophy. Volumetric assessment methods measure tissue atrophy, which typically follows early biochemical changes. An alternate MRI contrast mechanism to visualize the early pathological changes is T1rho (or "T-1-rho"), the spin lattice relaxation time constant in the rotating frame, which determines the decay of the transverse magnetization in the presence of a "spin-lock" radio-frequency field. Macromolecular changes (in plaques and tangles) that accompany early AD are expected to alter bulk water T1rho relaxation times. In this work, we measure T1rho MRI on patients with clinically diagnosed AD, MCI and in age-matched cognitively normal control subjects in order to compare T1rho values with changes in brain volume in the same regions of the brain and demonstrate that T1rho can potentially constitute an important biomarker of AD.
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PMID:T1rho MRI of Alzheimer's disease. 1847 42

Progressive HIV disease has been associated with loss of memory T cell responses to Ag. To better characterize and quantify long-lived memory T cells in vivo, we have refined an in vivo labeling technique to study the kinetics of phenotypically distinct, low-frequency CD8(+) T cell subpopulations in humans. HIV-negative subjects and antiretroviral-untreated HIV-infected subjects in varying stages of HIV disease were studied. After labeling the DNA of dividing cells with deuterated water ((2)H(2)O), (2)H-label incorporation and die-away kinetics were quantified using a highly sensitive FACS/mass spectrometric method. Two different populations of long-lived memory CD8(+) T cells were identified in HIV-negative subjects: CD8(+)CD45RA(-)CCR7(+)CD28(+) central memory (T(CM)) cells expressing IL-7Ralpha and CD8(+)CD45RA(+)CCR7(-)CD28(-) RA effector memory (T(EMRA)) cells expressing CD57. In pilot studies in HIV-infected subjects, T(CM) cells appeared to have a shorter half-life and reduced abundance, particularly in those with high viral loads; T(EMRA) cells, by contrast, retained a long half-life and accumulated in the face of progressive HIV disease. These data are consistent with the hypothesis that IL-7Ralpha(+) T(CM) cells represent true memory CD8(+) T cells, the loss of which may be responsible in part for the progressive loss of T cell memory function during progressive HIV infection.
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PMID:Central memory CD8+ T cells appear to have a shorter lifespan and reduced abundance as a function of HIV disease progression. 1852 54

Oxidative stress may underlie age-dependent memory loss and cognitive decline. Toxic aldehydes, including 4-hydroxy-2-nonenal (HNE), an end product of lipid peroxides, are known to accumulate in the brain in neurodegenerative disease. We have previously shown that mitochondrial aldehyde dehydrogenase 2 (ALDH2) detoxifies HNE by oxidizing its aldehyde group. To investigate the role of such toxic aldehydes, we produced transgenic mice, which expressed a dominant-negative form of ALDH2 in the brain. The mice had decreased ability to detoxify HNE in their cortical neurons and accelerated accumulation of HNE in the brain. Consequently, their lifespan was shortened and age-dependent neurodegeneration and hyperphosphorylation of tau were observed. Object recognition and Morris water maze tests revealed that the onset of cognitive impairment correlated with the degeneration, which was further accelerated by APOE (apolipoprotein E) knock-out; therefore, the accumulation of toxic aldehydes is by itself critical in the progression of neurodegenerative disease, which could be suppressed by ALDH2.
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PMID:Age-dependent neurodegeneration accompanying memory loss in transgenic mice defective in mitochondrial aldehyde dehydrogenase 2 activity. 1855 Jul 66


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