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)

An autopsied case of Pick's disease, having an extraordinary cerebral change in the anterior portion of Lobus frontalis and temporalis, was reported. Our case is a 71 year-old woman at death with a fourteen year history of chronic progressive dementia and mental deterioration, and it may be stressed that the existence lasted 8 years, over the latter half of clinical course, was depended on the tube feeding. The first symptoms suddenly appeared in 1964, 2 months after her husband's death of illness, when she was 57. She prepared the table for breakfast late at night, calculated wrongly in her domestic account book, and stole foods in the grocery. Two years later, her illness was diagnosed as presenile dementia by characteristic personality change and marked dilatation of anterior horn of lateral ventriculus. On admission to National Musashi Sanatorium, three years after the first symptoms' appearance, she presented restless walking, insomnia, memory loss, weakness of concentration, and high degree of disorientation. Particularly, it was noticeable that she behaved with bizzare contact. After 1970, tube feeding was introduced continuously, because of swallowing difficulty. Death occurred in July 1978 from a general weakness and a broncho-pneumonia, 14 years after the onset of the first symptoms. Autopsy revealed small and atrophied brain weighed 820 g. Cerebral cortical atrophy extended to frontal, temporal, insular, and parietal lobes, but right T-1 was relatively well preserved. On section, frontal and temporal ventriculus were remarkably enlarged and caudate nuclei were extremely atrophic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Pick's disease with long duration--an extraordinary cerebral change in the fore part of cerebrum]. 381 43

A plastic nervous system requires the ability not only to acquire and store but also to forget. Here, we report that musashi (msi-1) is necessary for time-dependent memory loss in C. elegans. Tissue-specific rescue demonstrates that MSI-1 function is necessary in the AVA interneuron. Using RNA-binding protein immunoprecipitation (IP), we found that MSI-1 binds to mRNAs of three subunits of the Arp2/3 actin branching regulator complex in vivo and downregulates ARX-1, ARX-2, and ARX-3 translation upon associative learning. The role of msi-1 in forgetting is also reflected by the persistence of learning-induced GLR-1 synaptic size increase in msi-1 mutants. We demonstrate that memory length is regulated cooperatively through the activation of adducin (add-1) and by the inhibitory effect of msi-1. Thus, a GLR-1/MSI-1/Arp2/3 pathway induces forgetting and represents a novel mechanism of memory decay by linking translational control to the structure of the actin cytoskeleton in neurons.
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PMID:Forgetting is regulated via Musashi-mediated translational control of the Arp2/3 complex. 2463 Jul 19