scholarly journals The depressed frail phenotype as a risk factor for mortality in older adults: a prospective cohort in Peru

Heliyon ◽  
2021 ◽  
pp. e08640
Author(s):  
Gabriel A.J. Vasquez-Goñi ◽  
Basilio M. Papuico-Romero ◽  
Diego Urrunaga-Pastor ◽  
Fernando M. Runzer-Colmenares ◽  
José F. Parodi
2017 ◽  
Vol 17 (11) ◽  
pp. 2124-2130 ◽  
Author(s):  
Hiromi Matsumoto ◽  
Chika Tanimura ◽  
Shinji Tanishima ◽  
Mari Osaki ◽  
Hisashi Noma ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 325-325
Author(s):  
Erin Harrell ◽  
Nelson Roque

Abstract One modifiable risk factor of dementia is cognitive inactivity. Given cognitive ability is closely tied to continual performance of instrumental activities of daily living, cognitive training programs continue to be explored as a way to boost cognition and allow older adults to remain independent longer. While the efficacy of cognitive training is controversial, identifying activities older adults are willing to limit in exchange for cognitive training provides valuable information in relation to designing cognitive training programs that appeal to older adults. Using a qualitative approach, this study highlights activities older adults (ages 64+) noted as contributing to decreased gameplay of a cognitive training program on a tablet device. We found that respondents (61%) noted playing less as a result of entertainment activities (i.e., reading and playing games), social activities (31%) and travel (27%). Findings have implications for device form factor in administering cognitive training and other programs.


Author(s):  
Naoki Saji ◽  
Hiroyuki Suzuki ◽  
Naomi Katayama ◽  
Hyuma Makizako ◽  
Yasue Uchida ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 142-143
Author(s):  
Svetlana Ukraintseva ◽  
Konstantin Arbeev ◽  
Hongzhe Duan ◽  
Igor Akushevich ◽  
Mary Feitosa ◽  
...  

Abstract Age is major risk factor for AD; however, relationships between aging and AD are not well understood. Decline in physiological resilience is universal feature of human aging that may also play role in AD. Aging-related pathways (such as IGF-I/P53/mTOR-mediated) that are involved in tissue resilience work in concert to decide outcomes of cell responses to stress/damage, such as survival, apoptosis, autophagy, etc. We hypothesized that interplay among genes in these pathways may influence AD risk as result of epistasis (GxG). We estimated effects of pairwise epistasis between SNPs in 53 genes from respective pathways on AD risk in the LLFS compared with other data (HRS, CHS, LOADFS). We found significant (fdr<0.05) GxG effects on AD risk in older adults across datasets. The SNP rs11765954 in CDK6 gene was involved in top GxG effects on AD in all datasets, when paired with SNPs in BCL2 and PPARGC1A. The CDK6 role in AD could be pleiotropic, depending on its activity in neurons: CDK6 expression is needed for DNA repair and neuronal survival; however, CDK6 overexpression may lead to the cell cycle reentry in postmitotic neurons resulting in apoptosis, which may contribute to neurodegeneration. CDK6 was earlier found to interfere with BCL2 effects on apoptosis, and with PPARGC1A effects on energy metabolism, which might contribute to observed GxG between these genes. We conclude that interactions among genes from biologically connected aging pathways may significantly influence AD risk. Uncovering such GxG effects has a potential to yield new genetic targets for AD prevention/treatment.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 491-491
Author(s):  
Stephen Thielke

Abstract Little research has characterized the natural history of weight change in older adults. Different changes may occur during aging and dying. We analyzed 18 years of weight measures from a cohort of 736,361 Veterans, all of whom had died at age 70 or older. We produced summary measures that accounted for both chronological age and number of years before death. Several clear population-level trends appeared. (1) The average weight of the sample declined across all ages at a rate of about 0.18 BMI points per year. (2) Starting about seven years before death, the amount of loss began to accelerate, reaching a decline of 0.75 BMI points in the year before death. (3) Changes in weight relative to years of remaining life were independent of chronologic age. People who died at age 70 experienced, on average, the same type and duration of terminal decline as did those who died at age 95. (4) The dying process involved a cumulative loss of about 1.3 BMI points. (5) The distribution of weights during advancing age both declined and narrowed. (6) Disproportionate deaths occurred at the lower BMI ranges (below a BMI of 24), and especially below 18, regardless of age. (7) The finding in #5 is explained by the entire cohort losing weight, with death of the thinnest members. These findings argue for examining survival time in studies of weight change. They indicate that weight loss may be a natural part of dying, rather than a risk factor for it.


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