Everyday-like memory for objects in ageing and Alzheimer's disease assessed in a visually complex environment: The role of executive functioning and episodic memory

2014 ◽  
Vol 10 (1) ◽  
pp. 33-58 ◽  
Author(s):  
Hélène Sauzéon ◽  
Bernard N'Kaoua ◽  
Prashant Arvind Pala ◽  
Mathieu Taillade ◽  
Sophie Auriacombe ◽  
...  
Author(s):  
J.S. Shaw ◽  
S.M.H. Hosseini

Findings that the brain is capable of plasticity up until old age have led to interest in the use of cognitive training as a potential intervention to delay the onset of dementia. However, individuals participating in training regimens differ greatly with respect to their outcomes, demonstrating the importance of considering individual differences, in particular age and baseline performance in a cognitive domain, when evaluating the effectiveness of cognitive training. In this review, we summarize existing literature on cognitive training in adults across the domains of episodic memory, working memory and the task-switching component of executive functioning to clarify the picture on the impact of age and baseline performance on cognitive training-related improvements. Studies targeting episodic memory induced greater improvements in younger adults with more intact cognitive abilities, explained in part by factors specific to episodic memory training. By contrast, older, lower baseline performance adults improved most in several studies targeting working memory in older individuals as well as in the majority of studies targeting executive functioning, suggesting the preservation of neural plasticity in these domains until very old age. Our findings can have important implications for informing the design of future interventions for enhancing cognitive functions in individuals at the prodromal stage of Alzheimer’s Disease and potentially delaying the clinical onset of Alzheimer’s Disease. Future research should more clearly stratify individuals according to their baseline cognitive abilities and assign specialized, skill-specific cognitive training regimens in order to directly answer the question of how individual differences impact training effectiveness.


2020 ◽  
Author(s):  
Ruchika Shaurya Prakash ◽  
Michael R. McKenna ◽  
Oyetunde Gbadeyan ◽  
Rebecca Andridge ◽  
Douglas W. Scharre ◽  
...  

AbstractINTRODUCTIONThe most well-studied biomarkers in AD are CSF amyloid beta-42 (Aβ42), tau, p-tau, and the ratio p-tau/Aβ42. The ratiometric measure of p-tau/Aβ42 shows the best diagnostic accuracy, and correlates reliably with metrics of cognition in unimpaired participants. However, no study has examined the impact of the CSF p-tau/Aβ42 ratio in predicting cognitive decline in both healthy and AD individuals in one sample. The goal of this study was to examine whether CSF-based p-tau/Aβ42 predicts changes in global cognitive functioning, episodic memory, and executive functioning over a two-year period in cognitively impaired older adults (CU), and in individuals with Mild Cognitive Impairment (MCI) and Alzheimer’s disease (AD).METHODSThis study involves secondary analysis of data from 1215 older adults available in the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Neuropsychological variables, collected at baseline, 6-month, 12-month, and 24-month follow-ups, included the Preclinical Alzheimer’s Cognitive Composite (PACC) to assess global cognitive functioning, ADNI-MEM to assess episodic memory functioning, and ADNI-EF to assess executive functioning. Linear mixed models were constructed to examine the effect of CSF p-tau/Aβ42, diagnostic group, and change over time (baseline, 6-month, 12-month, and 24-month) on cognitive scores.RESULTSCSF p-tau/Aβ42 ratios predicted worsening cognitive impairment, both on global cognition and episodic memory in individuals with MCI and AD, but not in CU older adults and predicted decline in executive functioning for all three diagnostic groups.DISCUSSIONOur study, including CU, MCI, and AD individuals, provides evidence for differential cognitive consequences of accumulated AD pathology based on diagnostic groups.


2006 ◽  
Vol 2 ◽  
pp. S388-S388
Author(s):  
Melissa Lamar ◽  
Felicia Goldstein ◽  
David J. Libon ◽  
Angela V. Ashley ◽  
James J. Lah ◽  
...  

GeroPsych ◽  
2014 ◽  
Vol 27 (4) ◽  
pp. 161-169 ◽  
Author(s):  
Nienke A. Hofrichter ◽  
Sandra Dick ◽  
Thomas G. Riemer ◽  
Carsten Schleussner ◽  
Monique Goerke ◽  
...  

Hippocampal dysfunction and deficits in episodic memory have been reported for both Alzheimer’s disease (AD) and major depressive disorder (MDD). Primacy performance has been associated with hippocampus-dependent episodic memory, while recency may reflect working memory performance. In this study, serial position profiles were examined in a total of 73 patients with MDD, AD, both AD and MDD, and healthy controls (HC) by means of CERAD-NP word list memory. Primacy performance was most impaired in AD with comorbid MDD, followed by AD, MDD, and HC. Recency performance, on the other hand, was comparable across groups. These findings indicate that primacy in AD is impaired in the presence of comorbid MDD, suggesting additive performance decrements in this specific episodic memory function.


2011 ◽  
Author(s):  
Beyon H. Miloyan ◽  
Justina Avila ◽  
Inna Ghajoyan ◽  
Jill Razani

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   


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