scholarly journals Improving older adults’ memory performance using prior task success.

2013 ◽  
Vol 28 (2) ◽  
pp. 340-345 ◽  
Author(s):  
Lisa Geraci ◽  
Tyler M. Miller
2011 ◽  
Author(s):  
Matthew L. Hughes ◽  
Tyler M. Miller ◽  
Lisa Geraci

Gerontology ◽  
2019 ◽  
Vol 65 (6) ◽  
pp. 649-658
Author(s):  
Patrick Lemaire ◽  
Jonas Gouraud ◽  
Poshita Nicolas

2014 ◽  
Vol 28 (3) ◽  
pp. 148-161 ◽  
Author(s):  
David Friedman ◽  
Ray Johnson

A cardinal feature of aging is a decline in episodic memory (EM). Nevertheless, there is evidence that some older adults may be able to “compensate” for failures in recollection-based processing by recruiting brain regions and cognitive processes not normally recruited by the young. We review the evidence suggesting that age-related declines in EM performance and recollection-related brain activity (left-parietal EM effect; LPEM) are due to altered processing at encoding. We describe results from our laboratory on differences in encoding- and retrieval-related activity between young and older adults. We then show that, relative to the young, in older adults brain activity at encoding is reduced over a brain region believed to be crucial for successful semantic elaboration in a 400–1,400-ms interval (left inferior prefrontal cortex, LIPFC; Johnson, Nessler, & Friedman, 2013 ; Nessler, Friedman, Johnson, & Bersick, 2007 ; Nessler, Johnson, Bersick, & Friedman, 2006 ). This reduced brain activity is associated with diminished subsequent recognition-memory performance and the LPEM at retrieval. We provide evidence for this premise by demonstrating that disrupting encoding-related processes during this 400–1,400-ms interval in young adults affords causal support for the hypothesis that the reduction over LIPFC during encoding produces the hallmarks of an age-related EM deficit: normal semantic retrieval at encoding, reduced subsequent episodic recognition accuracy, free recall, and the LPEM. Finally, we show that the reduced LPEM in young adults is associated with “additional” brain activity over similar brain areas as those activated when older adults show deficient retrieval. Hence, rather than supporting the compensation hypothesis, these data are more consistent with the scaffolding hypothesis, in which the recruitment of additional cognitive processes is an adaptive response across the life span in the face of momentary increases in task demand due to poorly-encoded episodic memories.


2010 ◽  
Author(s):  
Meg E. Anders ◽  
Steven A. Rogers ◽  
Deborah A. Lowe

2020 ◽  
Author(s):  
Francesca Farina ◽  
Marc Patrick Bennett ◽  
James William Griffith ◽  
Bert Lenaert

Evidence concerning the impact of fear of memory decline on health-related outcomes is limited. To determine the relationship between fear-avoidance of memory decline, quality of life and subjective memory in older adults using a novel scale to measure fear of memory decline. Sixty-seven older adults (59-81 years) completed a 23-item self-report questionnaire designed to capture experiential, cognitive and behavioral components of fear of memory decline, known as the fear and avoidance of memory decline (FAM) scale. Memory performance was assessed using the Wechsler Memory Scale (WMS-IV) and the Memory Failures Scale (MFS). General anxiety was assessed using the Depression, Anxiety and Stress Scales (DASS) and the Geriatric Anxiety Inventory (GAI). Quality of life was assessed using the Older Person’s Quality of Life scale (OPQOL-35). The FAM scale demonstrated good reliability and validity. Three latent factors were observed including: (1) fear-avoidance, (2) problematic beliefs and (3) resilience. After adjusting for age, education, memory performance and general anxiety, higher fear-avoidance predicted lower quality of life (p=.021) and increased memory failures (p=.022). Increased fear of memory decline predicts lower quality of life and subjective memory failures in healthy older adults. Based on these findings, we propose a preliminary fear-avoidance model that explains the development and maintenance of dementia-related functional disability in terms of psychological processes.


2021 ◽  
pp. 1-13
Author(s):  
Alexandra L. Clark ◽  
Alexandra J. Weigand ◽  
Kelsey R. Thomas ◽  
Seraphina K. Solders ◽  
Lisa Delano-Wood ◽  
...  

Background: Age-related cerebrovascular and neuroinflammatory processes have been independently identified as key mechanisms of Alzheimer’s disease (AD), although their interactive effects have yet to be fully examined. Objective: The current study examined 1) the influence of pulse pressure (PP) and inflammatory markers on AD protein levels and 2) links between protein biomarkers and cognitive function in older adults with and without mild cognitive impairment (MCI). Methods: This study included 218 ADNI (81 cognitively normal [CN], 137 MCI) participants who underwent lumbar punctures, apolipoprotein E (APOE) genotyping, and cognitive testing. Cerebrospinal (CSF) levels of eight pro-inflammatory markers were used to create an inflammation composite, and amyloid-beta 1–42 (Aβ 42), phosphorylated tau (p-tau), and total tau (t-tau) were quantified. Results: Multiple regression analyses controlling for age, education, and APOE ɛ4 genotype revealed significant PP x inflammation interactions for t-tau (B = 0.88, p = 0.01) and p-tau (B = 0.84, p = 0.02); higher inflammation was associated with higher levels of tau within the MCI group. However, within the CN group, analyses revealed a significant PP x inflammation interaction for Aβ 42 (B = –1.01, p = 0.02); greater inflammation was associated with higher levels of Aβ 42 (indicative of lower cerebral amyloid burden) in those with lower PP. Finally, higher levels of tau were associated with poorer memory performance within the MCI group only (p s <  0.05). Conclusion: PP and inflammation exert differential effects on AD CSF proteins and provide evidence that vascular risk is associated with greater AD pathology across our sample of CN and MCI older adults.


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