Characterizing cognitive aging of recognition memory and related processes in animal models and in humans

Burke, Sara N.; Ryan, Lee; Barnes, Carol A.

doi:10.3389/fnagi.2012.00015

Cited by 70 publications

(62 citation statements)

References 118 publications

(176 reference statements)

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“…9b), consistent with an age-dependent cognitive decline 35 . In contrast, the discrimination index of TgRln mice aged 12 months was significantly higher than that of the control group.…”

Section: Reelin Delays Ab Fibrillization and Extends Oligomer Lifetimementioning

confidence: 48%

Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

et al. 2014

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Reelin is an extracellular matrix protein that is crucial for neural development and adult brain plasticity. While the Reelin signalling cascade has been reported to be associated with Alzheimer's disease (AD), the role of Reelin in this pathology is not understood. Here we use an in vitro approach to show that Reelin interacts with amyloid-b (Ab 42 ) soluble species, delays Ab 42 fibril formation and is recruited into amyloid fibrils. Furthermore, Reelin protects against both the neuronal death and dendritic spine loss induced by Ab 42 oligomers. In mice carrying the APP Swe/Ind mutation (J20 mice), Reelin overexpression delays amyloid plaque formation and rescues the recognition memory deficits. Our results indicate that by interacting with Ab 42 soluble species, delaying Ab plaque formation, protecting against neuronal death and dendritic spine loss and preventing AD cognitive deficits, the Reelin pathway deserves consideration as a therapeutic target for the treatment of AD pathogenesis.

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“…9b), consistent with an age-dependent cognitive decline 35 . In contrast, the discrimination index of TgRln mice aged 12 months was significantly higher than that of the control group.…”

Section: Reelin Delays Ab Fibrillization and Extends Oligomer Lifetimementioning

confidence: 48%

Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

et al. 2014

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“…12 Interestingly, these regions convey novel object information to the hippocampus and are required for visual discrimination and object recognition memory. 13,14 PRC lesions have been found to impair visual discrimination between similar complex stimuli [15][16][17] and aging comes with deficits in PRC-dependent pattern separation in rodents and monkeys. 18 In contrast, the parahippocampal cortex and the medial entorhinal cortex convey information about spatial layouts and presumably aid context recall.…”

Section: Introductionmentioning

confidence: 98%

Vascular hippocampal plasticity after aerobic exercise in older adults

et al. 2014

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Aerobic exercise in young adults can induce vascular plasticity in the hippocampus, a critical region for recall and recognition memory. In a mechanistic proof-of-concept intervention over 3 months, we investigated whether healthy older adults (60-77 years) also show such plasticity. Regional cerebral blood flow (rCBF) and volume (rCBV) were measured with gadolinium-based perfusion imaging (3 Tesla magnetic resonance image (MRI)). Hippocampal volumes were assessed by high-resolution 7 Tesla MRI. Fitness improvement correlated with changes in hippocampal perfusion and hippocampal head volume. Perfusion tended to increase in younger, but to decrease in older individuals. The changes in fitness, hippocampal perfusion and volume were positively related to changes in recognition memory and early recall for complex spatial objects. Path analyses indicated that fitness-related changes in complex object recognition were modulated by hippocampal perfusion. These findings indicate a preserved capacity of the aging human hippocampus for functionally relevant vascular plasticity, which decreases with progressing age.

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“…As a result, representations of ambiguous stimuli in memory become highly susceptible to interference from external stimuli sharing similar features. Because of this interference, stimuli containing ambiguous features evoke a large number of false-positives on tests of recognition memory [11,18,19]. This interference effect is consistent with the ability to encode stimuli only at the simple feature level, as novel stimuli sharing features with the target stimulus become more likely to be perceived as familiar.…”

Section: Introductionmentioning

confidence: 60%

“…However, amnesic patients with damage that included the perirhinal cortex had difficulty discriminating between objects when the use of feature conjunctions was required, despite performing normally when discriminations only required the use of simple feature representations. These findings suggest that damage to the perirhinal cortex results in difficulty creating conjunctive representations [11,14,[16][17][18][19]. Without feature conjunctions, stimuli can only be encoded at the simple feature level.…”

Section: Introductionmentioning

confidence: 94%

Age-Related Deficits in Conjunctive Representation of Complex Objects

Scheerer¹,

Marrone²

2014

CAS

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Abstract:Although some evidence is consistent with the notion that distinct cortical systems support memory and perception, mounting evidence supports a representational-hierarchical view of cognition, which posits that distinctions lie in simple feature representations versus more complex conjunctive representations of many stimulus features simultaneously. Thus, typical memory tasks engage different regions from typical perception tasks because they inherently test information on opposing ends of this continuum. Memory deficits are reliably reported with age, but the tasks used to make these conclusions predominantly rely on conjunctive representations. To test the extent to which age-related deficits may be accounted for by perceptual processing, this study investigated discriminations involving conjunctive representations in older adults. Results show that adults aged 50 to 77 are impaired, relative to their younger counterparts, on discriminations requiring feature conjunctions, but not simple feature representations. These findings support recent data showing an agerelated decline in the ability to form conjunctive representations. Furthermore, these data suggest that some 'mnemonic' deficits associated with age may in fact be the result of deficits in perception rather than memory.

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Characterizing cognitive aging of recognition memory and related processes in animal models and in humans

Cited by 70 publications

References 118 publications

Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

Vascular hippocampal plasticity after aerobic exercise in older adults

Age-Related Deficits in Conjunctive Representation of Complex Objects

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