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Query: UMLS:C0598853 (forgetting)
 3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A model of memory retrieval is described. The model embodies 4 main claims: (a) temporal memory--traces of items are represented in memory partly in terms of their temporal distance from the present; (b) scale-similarity--similar mechanisms govern retrieval from memory over many different timescales; (c) local distinctiveness--performance on a range of memory tasks is determined by interference from near psychological neighbors; and (d) interference-based forgetting--all memory loss is due to interference and not trace decay. The model is applied to data on free recall and serial recall. The account emphasizes qualitative similarity in the retrieval principles involved in memory performance at all timescales, contrary to models that emphasize distinctions between short-term and long-term memory.
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PMID:A temporal ratio model of memory. 1763 96

A Heideggerian hermeneutical phenomenological research method was used to investigate the experience of memory loss in twelve individuals with early Alzheimer's disease or mild cognitive impairment. Data analysis proceeded as described by Diekelmann, Allen, and Tanner (1989), and incorporated the methods of Benner (1994), Thomas and Pollio (2002), and van Manen (1990). Three constitutive patterns with relational themes were identified. The first pattern, experiencing breakdown, consisted of two themes: awakening to breakdown and living with forgetting. The second pattern, temporality, consisted of three themes: being in the nothing, forgetting the past, and looking ahead. The third pattern, managing forgetting, consisted of the themes: remembering with cues, writing things down, recognizing what made remembering better or worse, and using laughter. The finding show that early Alzheimer's disease is more than an illness of cognitive losses and that forgetting is significant in light of the meaning that it has within everyday life.
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PMID:Losing one's memory in early Alzheimer's disease. 1858 8

A study was carried out to investigate accelerated forgetting of new verbal and visual material in participants complaining of memory loss, individuals with Mild Cognitive Impairment(MCI) and controls. All groups were evaluated with a standard neuropsychological battery and two tests of delayed recall 6 weeks apart for the experimental tasks.Individuals with memory complaints,but not MCI, performed normally compared to controls on immediate and 30 minute recall,but showed a striking impairment in verbal and visual memory after 6 weeks. Accelerated forgetting may go undetected on standard neuropsychological evaluation in some patients complaining of memory problems.
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PMID:Accelerated forgetting in subjects with memory complaints. A new form of Mild Cognitive Impairment? 1848 36

A key question in cognitive psychology is whether information in short-term memory is lost as a function of time. Lewandowsky, Duncan, and Brown (2004) argued against that memory loss because forgetting in serial recall occurred to the same extent across serial positions regardless of the rate of recall. However, we believe Lewandowsky et al. (2004) only prevented one of two types of rehearsal; they did not prevent nonarticulatory rehearsal via attention. To prevent articulatory and nonarticulatory rehearsal without introducing interference, we presented unevenly timed stimuli for serial recall and, on some trials, required that the timing of stimuli be reproduced in the response. In those trials only, evidence of memory loss over time emerged. Further research is needed to identify whether this memory loss is decay or lost distinctiveness.
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PMID:Short-term memory loss over time without retroactive stimulus interference. 1573 87

Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which the principle manifestation is recurrent, transient episodes of isolated memory loss. In addition to the amnesic episodes, many patients describe significant interictal memory difficulties. Performance on standard neuropsychological tests is often normal. However, two unusual forms of memory deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades. The neuroanatomical bases of TEA and its associated memory deficits are unknown. In this study, we first assessed the relationship between subjective and objective memory performance in 41 patients with TEA. We then analysed MRI data from these patients and 20 matched healthy controls, using manual volumetry and voxel-based morphometry (VBM) to correlate regional brain volumes with clinical and neuropsychological data. Subjective memory estimates were unrelated to performance on standard neuropsychological tests but were partially predicted by mood, ALF and remote autobiographical memory. Manual volumetry identified subtle hippocampal volume loss in the patient group. Both manual volumetry and VBM revealed correlations between medial temporal lobe atrophy and standard anterograde memory scores, but no relation between atrophy and ALF or remote autobiographical memory. These results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy. Furthermore, they suggest that although standard anterograde memory test performance is related to the degree of mesial temporal lobe damage, this is not true for ALF and autobiographical amnesia. It is possible that these unusual memory deficits have a more diffuse physiological basis rather than being a consequence of discrete structural damage.
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PMID:Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits. 1907 52

Initially acquired memory dissipates rapidly if not consolidated. Such memory decay is thought to result either from the inherently labile nature of newly acquired memories or from interference by subsequently attained information. Here we report that a small G protein Rac-dependent forgetting mechanism contributes to both passive memory decay and interference-induced forgetting in Drosophila. Inhibition of Rac activity leads to slower decay of early memory, extending it from a few hours to more than one day, and to blockade of interference-induced forgetting. Conversely, elevated Rac activity in mushroom body neurons accelerates memory decay. This forgetting mechanism does not affect memory acquisition and is independent of Rutabaga adenylyl cyclase-mediated memory formation mechanisms. Endogenous Rac activation is evoked on different time scales during gradual memory loss in passive decay and during acute memory removal in reversal learning. We suggest that Rac's role in actin cytoskeleton remodeling may contribute to memory erasure.
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PMID:Forgetting is regulated through Rac activity in Drosophila. 2017 38

Retrograde memory is frequently tested in the mental status examination of patients with stroke or degenerative dementia. The goal of this experiment was to compare gradients of retrograde memory in patients without neurologic disease (n = 26), patients with cerebrovascular disease (n = 43), and patients with probable Alzheimer's disease (n = 27). Patients were asked to recall and then name photographs of the 6 most recent US presidents. The free recall of patients with both cerebrovascular disease and probable Alzheimer's disease formed an exaggeration of the normal forgetting curve seen in control patients, in that the most recent presidents were most likely to be remembered. For photo naming, control patients showed essentially no forgetting, whereas patients with cerebrovascular disease or Alzheimer's disease had substantial memory loss with no temporal gradient. Alzheimer's disease caused significantly worse retrograde memory loss than did cerebrovascular disease, despite the two groups' equivalence in global intellectual functioning. Consistent with the focal or multifocal nature of cerebrovascular disease, stepwise multiple regression of retrograde memory on neuropsychological testing indicated that producing names by free recall was predicted by aphasic deficits, and that photo naming was predicted by visuoperceptual deficits. In Alzheimer's disease, free recall was predicted primarily by deficits in verbal new learning, consistent with amnesia, whereas photo naming was predicted by loss of general knowledge, consistent with dementia. The results are consistent with the idea that free recall of names from the past is a form of episodic memory, whereas naming of famous faces from the past is a form of semantic memory.
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PMID:Retrograde memory in cerebrovascular disease and Alzheimer's disease. 2128 67

Out-of-equilibrium disordered systems may form memories of external driving in a remarkable fashion. The system "remembers" multiple values from a series of training inputs yet "forgets" nearly all of them at long times despite the inputs being continually repeated. Here, learning and forgetting are inseparable aspects of a single process. The memory loss may be prevented by the addition of noise. We identify a class of systems with this behavior, giving as an example a model of non-Brownian suspensions under cyclic shear.
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PMID:Generic transient memory formation in disordered systems with noise. 2179 31

Transient epileptic amnesia (TEA) is a recently recognised syndrome of epilepsy in which the principle manifestation of seizures is recurrent episodes of isolated memory loss. In this article, we describe the clinical and cognitive profile of this emerging syndrome, and present new data that provide at most weak support for its proposed relationship to cerebrovascular disease. TEA is often associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting and remote memory impairment. We discuss the clinical and theoretical implications of these relatively novel cognitive deficits.
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PMID:The causes and consequences of transient epileptic amnesia. 2206 18

Although forgetting is most often thought of in terms of declines in performance (response loss or impairment), another class of memory phenomena, the forgetting of stimulus attributes, has begun to attract experimental attention. In non-human animals, the loss of memory for stimulus features is reflected in the flattening of stimulus generalization gradients as well as in the attenuation of the disrupting effect of a shift in context at testing. In both cases, a delay between the learning episode and testing results in increased responding in the presence of previously ineffective stimuli. Thus, previously discriminable cues become more functionally interchangeable. The implications of the forgetting of attributes for some theoretical issues of memory loss and for methodological strategies have been noted earlier. However, relatively little is known about the neurobiological mechanisms underlying stimulus attribute forgetting, and why some memories are maintained while others are not. In this paper we review the evidence for the forgetting of stimulus attributes, discuss recent findings identifying neurobiological underpinnings of forgetting and generalization of fear responses, and discuss relevant clinical implications of fear generalization.
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PMID:Remembering another aspect of forgetting. 2267 15


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