Forgetting of pictures over a long retention interval in young and older adults.

Park, Denise C.; Royal, Derek Parker; Dudley, William; Morrell, R.

doi:10.1037/0882-7974.3.1.94

Cited by 41 publications

(31 citation statements)

References 6 publications

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“…Aging in humans is associated with a weakening of working memory, executive function, and processing speed; however, the most notable decline is observed as impaired episodic memory, including spatial memory (Kukolja et al , 2009; Plancher et al , 2010; Uttl and Graf, 1993). The impairment can be identified as a mild deficit in the rapid acquisition of flexible information and an increase in the rate of forgetting (Davis et al , 2003; Hogge et al , 2008; Huppert and Kopelman, 1989; Kral, 1962; Macdonald et al , 2006; Mitchell et al , 1990; Park et al , 1988; Rajah et al , 2010). …”

Section: Introductionmentioning

confidence: 99%

Dissecting the age-related decline on spatial learning and memory tasks in rodent models: N-methyl-D-aspartate receptors and voltage-dependent Ca2+ channels in senescent synaptic plasticity

Foster

2012

Progress in Neurobiology

147

157

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In humans, heterogeneity in the decline of hippocampal-dependent episodic memory is observed during aging. Rodents have been employed as models of age-related cognitive decline and the spatial water maze has been used to show variability in the emergence and extent of impaired hippocampal-dependent memory. Impairment in the consolidation of intermediate-term memory for rapidly acquired and flexible spatial information emerges early, in middle-age. As aging proceeds, deficits may broaden to include impaired incremental learning of a spatial reference memory. The extent and time course of impairment has been be linked to senescence of calcium (Ca2+) regulation and Ca2+-dependent synaptic plasticity mechanisms in region CA1. Specifically, aging is associated with altered function of N-methyl-D-aspartate receptors (NMDARs), voltage-dependent Ca2+ channels (VDCCs), and ryanodine receptors (RyRs) linked to intracellular Ca2+ stores (ICS). In young animals, NMDAR activation induces long-term potentiation of synaptic transmission (NMDAR-LTP), which is thought to mediate the rapid consolidation of intermediate-term memory. Oxidative stress, starting in middle-age, reduces NMDAR function. In addition, VDCCs and ICS can actively inhibit NMDAR-dependent LTP and oxidative stress enhances the role of VDCC and RyR-ICS in regulating synaptic plasticity. Blockade of L-type VDCCs promotes NMDAR-LTP and memory in older animals. Interestingly, pharmacological or genetic manipulations to reduce hippocampal NMDAR function readily impair memory consolidation or rapid learning, generally leaving incremental learning intact. Finally, evidence is mounting to indicate a role for VDCC-dependent synaptic plasticity in associative learning and the consolidation of remote memories. Thus, VDCC-dependent synaptic plasticity and extrahippocampal systems may contribute to incremental learning deficits observed with advanced aging.

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Section: Introductionmentioning

confidence: 99%

Dissecting the age-related decline on spatial learning and memory tasks in rodent models: N-methyl-D-aspartate receptors and voltage-dependent Ca2+ channels in senescent synaptic plasticity

Foster

2012

Progress in Neurobiology

147

157

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“…The impairments often take the form of rapid forgetting of recently learned information in both humans (Gagnon and Belleville, 2011; Huppert and Kopelman, 1989; Munro Cullum et al, 1990; Park et al, 1988) and rodents (Barnes, 1991; Countryman and Gold, 2007; Foster, 1999; Gold, 2005, 2008; Gold et al, 1982; Korol, 2002; Quartermain et al, 1988; Salinas and Gold, 2005; Winocur, 1988; Zornetzer et al, 1982). Previous work in rodents suggests that rapid forgetting may reflect deficits in neurobiological mechanisms of memory formation initiated during or soon after training.…”

Section: Introductionmentioning

confidence: 99%

Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: Relationships to age-related memory impairments

Morris

Gold

2013

Experimental Gerontology

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Epinephrine enhances memory in young adult rats, in part, by increasing blood glucose levels needed to modulate memory. In old rats, epinephrine is deficient at raising blood glucose levels and thus is only moderately effective at enhancing memory. In contrast, systemic glucose injections improve memory in old rats, with resulting memory performance equal to that of young rats. The diminished response of glucose to training in old rats may blunt downstream neurochemical and molecular mechanisms needed to upregulate memory processes. In the first experiment, young adult and old rats were trained on an inhibitory avoidance task with immediate post-training injections of aCSF or glucose into the dorsal hippocampus. Old rats had significant memory impairments compared to young rats 7 days after training. Intrahippocampal injections of glucose reversed age-related deficits, improving memory scores in old rats to values seen in young rats. A second experiment examined age-related changes in activation of the transcription factor CREB, which is widely implicated in memory formation and may act downstream of hormonal and metabolic signals. Activation was assessed in response to training with systemic injections of epinephrine and glucose at doses known to enhance memory. Young adult and old rats were trained on inhibitory avoidance with immediate post-training systemic injections of saline, epinephrine, or glucose. After training, old rats had significant impairments in CREB phosphorylation in area CA1 and the dentate gyrus region of the hippocampus, and in the basolateral and lateral amygdala. Epinephrine and glucose attenuated age-related deficits in CREB phosphorylation, but were more effective in the amygdala and hippocampus, respectively. Together, these results support the view that age-related changes in blood glucose responses to epinephrine contribute to memory impairments, which may be related to alterations in regional patterns of CREB phosphorylation.

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“…In aging research, forgetting rates have been studied across different age groups and retention intervals and the findings are mixed. Whereas some studies reported differences in initial performance, but invariant forgetting rates in older and younger adults (Fjell et al, 2005;Rybarczyk, Hart, & Harkins, 1987;Spikman, Berg, & Deelman, 1995), others have shown greater forgetting in older adults, especially after long delays (e.g., 1 week; see Huppert & Kopelman, 1989;Park, Royal, Dudley, & Morrell, 1988), or when testing individuals on episodic recall, rather than recognition tasks (MacDonald, Stigsdotter-Neely, et al, 2006). With respect to experimental manipulations, encoding factors such as meaningfulness of the material (Underwood & Richardson, 1956), degree of learning (Slamecka & McElree, 1983), and pictorial elaboration (Forbes & Reese, 1974) have been found to affect initial rate of learning, but not rate of forgetting.…”

Section: Interindividual Differences In Forgettingmentioning

confidence: 99%

Higher intraindividual variability is associated with more forgetting and dedifferentiated memory functions in old age

et al. 2011

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a b s t r a c tIntraindividual trial-to-trial reaction time (RT) variability is commonly found to be higher in clinical populations or life periods that are associated with impaired cognition. In the present study, higher within-person trial-to-trial RT variability in a perceptual speed task is related to more forgetting and dedifferentiation of memory functions in older adults (aged 60-71 years). More specifically, our study showed that individuals in a high-variability group (n = 175) forgot more memory scenes over a 1-week retention interval than individuals in the low-variability group (n = 174). In contrast, slower RT speed was associated with poorer episodic memory in general, but unrelated to the amount of forgetting. Moreover, results from multiple group latent factor analyses showed that episodic memory and working memory functions were more highly correlated in the high-variability (r = .63) than in the low-variability (r = .25) group. Given that deficits in dopamine (DA) modulation may underlie increases in RT variability, the present findings are in line with (i) recent animal studies implicating DA in long-term episodic memory consolidation and (ii) neurocomputational work linking DA modulation of performance variability to dedifferentiation of cognitive functions in old age.

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Forgetting of pictures over a long retention interval in young and older adults.

Cited by 41 publications

References 6 publications

Dissecting the age-related decline on spatial learning and memory tasks in rodent models: N-methyl-D-aspartate receptors and voltage-dependent Ca2+ channels in senescent synaptic plasticity

Dissecting the age-related decline on spatial learning and memory tasks in rodent models: N-methyl-D-aspartate receptors and voltage-dependent Ca2+ channels in senescent synaptic plasticity

Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: Relationships to age-related memory impairments

Higher intraindividual variability is associated with more forgetting and dedifferentiated memory functions in old age

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