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)

Previous studies have shown that following an acute bout of pyrithiamine-induced thiamine deficiency (PTD) rats are impaired in learning appetitively and aversively motivated T-maze tasks. The present study examined if PTD-treated rats exhibit both anterograde and retrograde memory loss of an aversively motivated spatial navigation task. Histological examination revealed two consistent lesions in the PTD treated rats: a bilateral, symmetrical destruction of medial thalamus centered on the internal medullary lamina (IML), and a lesion of the medial nucleus of the mammillary body. In Experiment 1, control and recovered PTD rats were trained to find a hidden platform in a Morris water maze. PTD rats with the IML lesion were impaired in learning the water maze task but were eventually able to perform as well as controls and PTD animals without the IML lesion. In Experiment 2, half of the pretrained CT animals underwent thiamine deficiency (PTD2), were recovered, and subsequently were tested for retention of the platform location. The remaining CT animals and the PTD1 group were also tested for retention. No significant group differences were observed on any of the four postretention trials. When compared to their performance on the last four preretention trials, the performance of PTD1 and PTD2 animals with IML lesions were similar to those of the controls. These results demonstrate that acute thiamine deficiency in rats produces damage of medial thalamic and mammillary body nuclei, a mild anterograde learning deficit, but no loss of retrograde memory of the Morris water maze task.
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PMID:Diencephalic lesions, learning impairments, and intact retrograde memory following acute thiamine deficiency in the rat. 161 8

Insomnia, a common complaint among the elderly, is generally treated with benzodiazepines. Long-acting benzodiazepines (e.g., flurazepam) often produce daytime somnolence and performance deficits, whereas short-acting drugs (e.g., triazolam) have been associated with marked rebound insomnia and anterograde memory loss. The authors designed a pilot study to evaluate the efficacy of an intermediate-acting benzodiazepine, estazolam (e.g., ProSom), as well as its side effects. The parameters studied were sleep, daytime performance, and memory. Ten geriatric patients (greater than 60 years of age) with insomnia participated in the study. They received placebo nightly for 2 weeks (baseline), estazolam 1 mg nightly for the next 4 weeks (treatment phase), and placebo again for 2 weeks (withdrawal period). Sleep was monitored by polysomnography the first two nights of each week in a sleep laboratory. Estazolam significantly decreased sleep latency, nocturnal awakenings, and wake time after sleep onset. Total sleep time increased an average of 63 minutes the first night of treatment. Significant improvements in wake time after sleep onset and total sleep time also were observed in the fourth week of estazolam treatment. Rebound insomnia occurred on the first withdrawal night only for wake time and total sleep time. By the next night, these sleep parameters returned to baseline. Neither day-time performance nor anterograde memory was adversely affected by estazolam treatment or its withdrawal. A 1-mg dose of estazolam appears to be a safe and effective hypnotic for elderly patients with insomnia.
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PMID:The effects of estazolam on sleep, performance, and memory: a long-term sleep laboratory study of elderly insomniacs. 164 5

What makes our own aging so interesting and predictions about normative aging profiles so difficult is that there are many different capacities that may be altered. The composite pattern of strengths and needs and of the degree of need has yet to be described. This makes predictions about what people can or could do difficult. Each individual represents a mosaic of capacity and loss resulting from the impact of capacities such as vision, hearing, response time, posture, gait, energy level, and even recall and the demands placed upon them by their individual circumstances, life-styles, and environments. A person with major memory loss and tremendous energy may be different from one who experiences slight losses in vision, hearing, mobility, agility, and a crystal clear memory. Their behavioral changes may be more evident in strange environments than in familiar ones. This mosaic of capabilities and needs makes traditional interventions that are focused on a singular disability or major diagnostic conditions difficult. Traditional rehabilitation methods need to be adapted to grapple with the diversity of older people functioning in a community. Adaptations in our understanding of people, activities, and environments will put us in a better position to facilitate the normal interactions of older people in senior centers and, importantly, in public intergenerational settings. Older people have not been well served by services, programs, and legislation that have focused on single disabilities or devices.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Shaping a life-style of independence. Abilities, aging, and environmental design. 164 Mar 76

In recent years there has been an increased interest in understanding the role of somatostatin in the brain. This review summarizes the current knowledge of the anatomical distribution of somatostatin and its receptors, the receptor-coupling mechanisms and the somatostatinergic modulation of cognitive functions. Somatostatin is also highly concentrated in the extra-hypothalamic areas of the brain, including the frontal and parietal cortex and the hippocampus. At these locations somatostatin may play a fundamental role in the modulation of cognitive functions. Activation of somatostatin receptors in the brain results in an inhibition of adenylate cyclase enzyme activity, reduction in intracellular Ca2+ levels and hypopolarization of cells by inducing outward K+ currents. Biological studies on the effects of increased brain somatostatin showed a facilitation in learning behavioural tasks, while brain somatostatin depletion by cysteamine caused memory loss. These observations, along with the severe somatostatinergic neurotransmission impairment demonstrated in Alzheimer's patients, strongly suggest a fundamental role for somatostatin in the modulation of cognitive functions.
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PMID:Brain somatostatin: receptor-coupled transducing mechanisms and role in cognitive functions. 164 19

Neurosarcoidosis is a well-recognised complication of systemic sarcoidosis but diagnosis may be difficult if there is no clear evidence of an extracerebral manifestation of the disease. We present the case of a 42-year-old woman with clinical features characteristic of cerebral sarcoidosis including tetraparesis, diabetes insipidus, diencephalic hyperphagia, personality changes, and memory loss. Diagnosis was supported by cerebrospinal fluid (CSF) findings and magnetic resonance imaging (MRI): CSF showed mild lymphocytic pleocytosis, intrathecal production of IgG without oligoclonal bands, and a raised level of lysozyme. MRI revealed multiple contrast-enhanced granulomas at the base of the brain with partial involvement of diencephalic and mesencephalic structures and parts of the spinal cord. There was no evidence of systemic manifestation of sarcoidosis. Administration of corticosteroids led to improvement of the symptoms.
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PMID:Neurosarcoidosis without systemic sarcoidosis. 165 87

A 59-year-old demented Japanese man who was proven to have high titer of serum alpha-fetoprotein (AFP) and carcino-embryonic antigen (CEA) was admitted to our hospital. Neurological examinations revealed moderate dementia with deterioration and loss of memory, and decreased deep tendon reflexes in all extremities. Sensory disturbances were not obvious. There were no significant changes in the usual laboratory findings including CSF, except for elevated serum AFP and CEA. Three months after admission, he died of gastric cancer and its metastases in liver and lymph nodes. Post-mortem examination in the central nervous system (CNS) revealed many senile plaques and neurofibrillary tangles throughout the cerebral cortex and hippocampus. There was marked loss of neurons in the hippocampus. All the neuropathological findings in the CNS were consistent with those in Alzheimer disease. In the peripheral nervous system, necrotizing arteritis was found throughout the length of sciatic nerve. Large myelinated fibers seemed to be preferentially degenerated with proximo-distal gradient. Teased fiber preparation revealed de/remyelination and axonal degeneration more frequently at the distal portion. Immunohistologically, the serum IgG of this patient specifically reacted to the endothelial cells of all vessels in control organs, which strongly suggested the autoimmune mechanism for the necrotizing arteritis in this patient. The pathogenetic role of this antibody for necrotizing arteritis, found selectively in the peripheral nervous system, still remained unclear. However, paraneoplastic neuropathy due to necrotizing arteritis is a distinct entity in addition to common form of paraneoplastic subacute sensory neuropathy.
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PMID:[A case of paraneoplastic neuropathy with necrotizing arteritis localized in the peripheral nervous system]. 165 26

Senile dementia of Lewy body type is characterized clinically by a relatively acute onset of fluctuating memory loss and confusion, frequently accompanied by visual hallucinations. Neurochemical analyses of temporal cortex has revealed a distinction between hallucinating and nonhallucinating patients in both cholinergic and monaminergic transmitter activities. In contrast with the cholinergic enzyme choline acetyltransferase, which was more extensively reduced in hallucinating individuals, serotonergic S2 receptor binding and both dopamine and serotonin metabolites were significantly decreased in nonhallucinating cases. These results suggest that an imbalance between monaminergic and cholinergic transmitters is involved in hallucinogenesis in the human brain.
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PMID:Evidence of a monoaminergic-cholinergic imbalance related to visual hallucinations in Lewy body dementia. 169 97

Bilateral occlusion of the foramina of Monro was detected and treated in a hydrocephalic adult who developed rapid striking recent memory loss. She was treated by midline windowing of the third ventricle into the dilated lateral ventricles at a location 2 cm posterior to the occluded foramina of Monro. No inflammation was present. A biopsy specimen showed no evidence of malignancy. A reservoir was placed for long-term measurement of intraventricular pressure. Ten-year follow-up with pressure measurements, serial computed tomography scans, and magnetic resonance imaging showed no evidence of tumor.
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PMID:Adult "congenital" bilateral occlusion of the foramina of Monro. 172 84

Alzheimer's disease produces regional abnormalities in brain blood flow and metabolism that may result in recognizable scintigraphic patterns. We determined the predictive value of 99mTc-HMPAO SPECT for the presence of Alzheimer's disease based on a prospective study of 132 consecutive patients coming to our nuclear medicine clinical unit for evaluation of their memory loss or cognitive abnormalities. During clinical follow-up averaging 10.1 mo, a final diagnosis was established in 113 patients, 52 of which had Alzheimer's disease. The probability of Alzheimer's disease was determined for seven scintigraphic patterns. The probability was 19% that patients with memory loss and normal perfusion had Alzheimer's disease. For abnormal perfusion patterns, the probability of Alzheimer's disease was 82% with bilateral temporoparietal defects, 77% with bilateral temporoparietal defects with additional defects, 57% with unilateral temporoparietal defects, 43% with frontal defects only, 18% with other large defects and 0% with multiple small cortical defects. We conclude that for 99mTc-HMPAO SPECT the predictive value of bilateral temporoparietal defects for Alzheimer's disease is high, while the perfusion patterns of unilateral temporoparietal perfusion defects and frontal defects only, which occur in 20% of patients with Alzheimer's disease, are not predictive of that disease.
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PMID:The scintigraphic appearance of Alzheimer's disease: a prospective study using technetium-99m-HMPAO SPECT. 173 62

The clinical and pathologic features of 15 new cases of the uncommon primary or granulomatous angiitis of the central nervous system (PACNS) are described. To date, only 108 such cases have been reported in the English literature. Clinically, most PACNS patients have been young or middle-aged (mean age, 45 years; range, 3 to 96 years), with men outnumbering women slightly by a ratio of 4 to 3. The most frequent presenting complaints are headache, weakness, and confusion; less common complaints are aphasia, dysphasia, nausea or vomiting, loss of memory, and seizure disorder. There is usually no evidence of a systemic disease; the erythrocyte sedimentation rate is almost invariably normal, and there are no diagnostic laboratory tests. The cerebral angiogram usually shows multifocal, segmental stenosis or irregularity of small and medium-sized leptomeningeal and intracranial blood vessels, often with a beading or aneurysmal appearance, and alterations in blood flow in the affected regions. Anatomically, the angiitis is focal and segmental in distribution. An isolated negative biopsy, therefore, does not rule out the disease. Histologically, PACNS may be granulomatous, necrotizing, or lymphocytic in character, and mixed morphologic types often occur. Large- and small-vessel thrombosis is common. Acute lesions frequently coexist with healing or healed lesions. Involvement of extracranial blood vessels occurs only rarely. Past or current herpes zoster infection and Hodgkin's lymphoma are the most noteworthy clinical associations of PACNS, but whether they are causally related remains uncertain.
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PMID:Primary (granulomatous) angiitis of the central nervous system: a clinicopathologic analysis of 15 new cases and a review of the literature. 174 Mar


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