scholarly journals Brain morphology, cognition, and β-amyloid in older adults with superior memory performance

2018 ◽  
Vol 67 ◽  
pp. 162-170 ◽  
Author(s):  
Theresa M. Harrison ◽  
Anne Maass ◽  
Suzanne L. Baker ◽  
William J. Jagust
2017 ◽  
Vol 13 (7) ◽  
pp. P1463-P1464 ◽  
Author(s):  
Theresa M. Harrison ◽  
Samuel N. Lockhart ◽  
Suzanne L. Baker ◽  
William J. Jagust

Author(s):  
Christa Dang ◽  
Nawaf Yassi ◽  
Karra D. Harrington ◽  
Ying Xia ◽  
Yen Ying Lim ◽  
...  

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.


2021 ◽  
pp. 019394592110297
Author(s):  
Graham J. McDougall ◽  
Todd B. Monroe ◽  
Keenan A. Pituch ◽  
Michael A. Carter ◽  
Laurie Abbott

Cultural stereotypes that equate aging with decreased competence and increased forgetfulness have persisted for decades. Stereotype threat (ST) refers to the psychological discomfort people experience when confronted by a negative, self-relevant stereotype in a situation where their behavior could be construed as confirming that belief. The purpose of this study was to examine the relationships of ST on memory performance in older adults over 24 months. The ST levels on average significantly declined, or improved in the memory training, but not the health training group. Although not significant at the .01 level, the bivariate correlation indicated that change in ST was moderately related to change in verbal memory, suggesting the possibility that improvements (or reductions) in ST may be related to increases in verbal memory scores. We discovered that the unique contribution of ST into the memory performance of healthy older adults offers a possible malleable trait.


Brain ◽  
2021 ◽  
Author(s):  
David Berron ◽  
Jacob W Vogel ◽  
Philip S Insel ◽  
Joana B Pereira ◽  
Long Xie ◽  
...  

Abstract In Alzheimer’s disease, postmortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with area 35, and the entorhinal cortex. Here we used tau-PET imaging to investigate the sequence of tau pathology progression within the human medial temporal lobe and across regions in the posterior-medial system. Our objective was to study how medial temporal tau is related to functional connectivity, regional atrophy, and memory performance. We included 215 β-amyloid negative cognitively unimpaired, 81 β-amyloid positive cognitively unimpaired and 87 β-amyloid positive individuals with mild cognitive impairment, who each underwent [18]F-RO948 tau and [18]F-flutemetamol amyloid PET imaging, structural T1-MRI and memory assessments as part of the Swedish BioFINDER-2 study. First, event-based modelling revealed that the entorhinal cortex and area 35 show the earliest signs of tau accumulation followed by the anterior and posterior hippocampus, area 36 and the parahippocampal cortex. In later stages, tau accumulation became abnormal in neocortical temporal and finally parietal brain regions. Second, in cognitively unimpaired individuals, increased tau load was related to local atrophy in the entorhinal cortex, area 35 and the anterior hippocampus and tau load in several anterior medial temporal lobe subregions was associated with distant atrophy of the posterior hippocampus. Tau load, but not atrophy, in these regions was associated with lower memory performance. Further, tau-related reductions in functional connectivity in critical networks between the medial temporal lobe and regions in the posterior-medial system were associated with this early memory impairment. Finally, in patients with mild cognitive impairment, the association of tau load in the hippocampus with memory performance was partially mediated by posterior hippocampal atrophy. In summary, our findings highlight the progression of tau pathology across medial temporal lobe subregions and its disease-stage specific association with memory performance. While tau pathology might affect memory performance in cognitively unimpaired individuals via reduced functional connectivity in critical medial temporal lobe-cortical networks, memory impairment in mild cognitively impaired patients is associated with posterior hippocampal atrophy.


2021 ◽  
Author(s):  
Adeline Jabès ◽  
Giuliana Klencklen ◽  
Paolo Ruggeri ◽  
Christoph M. Michel ◽  
Pamela Banta Lavenex ◽  
...  

AbstractAlterations of resting-state EEG microstates have been associated with various neurological disorders and behavioral states. Interestingly, age-related differences in EEG microstate organization have also been reported, and it has been suggested that resting-state EEG activity may predict cognitive capacities in healthy individuals across the lifespan. In this exploratory study, we performed a microstate analysis of resting-state brain activity and tested allocentric spatial working memory performance in healthy adult individuals: twenty 25–30-year-olds and twenty-five 64–75-year-olds. We found a lower spatial working memory performance in older adults, as well as age-related differences in the five EEG microstate maps A, B, C, C′ and D, but especially in microstate maps C and C′. These two maps have been linked to neuronal activity in the frontal and parietal brain regions which are associated with working memory and attention, cognitive functions that have been shown to be sensitive to aging. Older adults exhibited lower global explained variance and occurrence of maps C and C′. Moreover, although there was a higher probability to transition from any map towards maps C, C′ and D in young and older adults, this probability was lower in older adults. Finally, although age-related differences in resting-state EEG microstates paralleled differences in allocentric spatial working memory performance, we found no evidence that any individual or combination of resting-state EEG microstate parameter(s) could reliably predict individual spatial working memory performance. Whether the temporal dynamics of EEG microstates may be used to assess healthy cognitive aging from resting-state brain activity requires further investigation.


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