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

I reanalyze the free recall data of Murdock, J Exp Psychol 64(5):482-488 (1962) and Murdock and Okada, J Verbal Learn and Verbal Behav 86:263-267 (1970) which show the famous bowing effect in which initial and recent items are recalled better than intermediate items (primacy and recency effects). Recent item recall probabilities follow a logarithmic decay with time of recall consistent with the tagging/retagging theory. The slope of the decay increases with increasing presentation rate. The initial items, with an effectively low presentation rate, decay with the slowest logarithmic slope, explaining the primacy effect. The finding that presentation rate limits the duration of short term memory suggests a basis for memory loss in busy adults, for the importance of slow music practice, for long term memory deficiencies for people with attention deficits who may be artificially increasing the presentation rates of their surroundings. A well-defined, quantitative measure of the primacy effect is introduced.
Cogn Neurodyn 2010 Dec
PMID:Short term memory bowing effect is consistent with presentation rate dependent decay. 2213 46

Thalidomide is a widely prescribed immunomodulatory drug (iMiD) for multiple myeloma, but causes reversible memory loss in humans. However, how thalidomide causes cognitive dysfunction at a cellular and molecular level has not been demonstrated. We studied the effect of thalidomide on synaptic functions and cognitive behaviors using a mouse model. Thalidomide led to cognitive deficits in learning behavior in a passive avoidance test and in a novel object recognition test, increased anxiety in an elevated plus maze test, and increased depressive behaviors in a tail suspension test. Interestingly, thalidomide elevated big- or large-conductance, calcium-activated K+ (BK) channel expression in the plasma membrane and BK channel activity in the hippocampus. Thalidomide also increased the paired pulse ratio of excitatory postsynaptic current (EPSC), which suggests a decreased probability of glutamate release. Furthermore, the changes in the paired pulse ratio and in BK channel activity were blocked by paxilline, a BK channel blocker. Finally, we found that thalidomide-induced cognitive dysfunctions were restored by paxilline treatment. These results suggest that thalidomide-mediated BK channel hyperfunction is responsible for the pathological mechanism of thalidomide-associated reversible memory loss.
 ...
PMID:BK channel blocker paxilline attenuates thalidomide-caused synaptic and cognitive dysfunctions in mice. 3051 85