The Association Between High-Molecular-Weight Adiponectin, Ghrelin and Leptin and Age-Related Cognitive Decline: Results From Longitudinal Aging Study Amsterdam

2020 ◽  
Vol 76 (1) ◽  
pp. 131-140
Author(s):  
Merel van Andel ◽  
Natasja M van Schoor ◽  
Nicole C Korten ◽  
Hannie C Comijs ◽  
Annemieke C Heijboer ◽  
...  

Abstract Background Age-related cognitive decline has large-scale functional and economic consequences and understanding its’ pathophysiological mechanisms is therefore essential. Previous research has suggested associations between hormones adiponectin, ghrelin and leptin and neurodegenerative disease. However, their association with age-related cognitive decline has not been fully described. We examine the association between serum high-molecular-weight (HMW) adiponectin, ghrelin and leptin and age-related cognitive decline in older adults. Methods The associations between HMW adiponectin, ghrelin and leptin and the Mini-Mental-State-Examination, Coding task (Coding), 15 Words Test (15WT) and composite Z-score (general cognitive function) were analyzed by means of a sex-stratified multivariable linear regression analysis in a population-based cohort of 898 older adults at baseline and after 3 years of follow-up. Results In women, we found a positive association between HMW adiponectin and general cognitive function at baseline (fully adjusted model composite Z-score standardized regression co-efficient beta [β] = .089, p = .025). After 3 years of follow-up, HMW adiponectin was associated with more decline in general cognitive function and information processing speed (fully adjusted model composite Z-score β = −.123, p = .018; Coding β = −.116, p = .027). Ghrelin and leptin were significantly associated with memory in a baseline subgroup analysis of older women. For men, we found no significant associations at baseline or follow-up. Conclusion Our results show variable associations between hormones HMW adiponectin, ghrelin and leptin and age-related cognitive decline in women but not in men. As there was no clear trend, all our results should be interpreted with caution.

2011 ◽  
Vol 17 (3) ◽  
pp. 315-324 ◽  
Author(s):  
O J G Schiepers ◽  
S E Harris ◽  
A J Gow ◽  
A Pattie ◽  
C E Brett ◽  
...  

2011 ◽  
Vol 23 (9) ◽  
pp. 1405-1412 ◽  
Author(s):  
Ralitsa Stoykova ◽  
Fanny Matharan ◽  
Jean-François Dartigues ◽  
Hélène Amieva

ABSTRACTBackground: The objective of this study was to investigate the relationship between social network and cognitive decline, taking into account the potential bias of reverse causality.Methods: The study sample comprised 2055 elderly participants without dementia. We assessed baseline social functioning across four variables: size of social network, satisfaction with relationships, perception of being understood, and participation in social activities. A neuropsychological battery was proposed at baseline and repeated throughout follow-up. Linear mixed models were used to investigate the relationship between social network and baseline cognitive performances and cognitive decline during the 20-year follow-up.Results: When controlling for the reverse causality bias by excluding participants who developed dementia during the study follow-up and after adjusting for covariates, the results showed that better social functioning at baseline was associated with better initial performances in the Isaacs Set Test and the Wechsler Paired Associate Test. However, there was no significant association with further cognitive decline. By contrast, when the bias of reverse causality was not controlled for (i.e. no exclusion of participants who developed dementia), the association between social network and global cognitive decline measured by MMSE was found to be statistically significant.Conclusion: With the opportunity to exclude participants who developed dementia, and the particularly long follow-up of participants, we were able to investigate the relationship between social networks and age-related cognitive decline with a minimization of reverse causality bias. The results suggest that even though higher social functioning is concomitantly associated with better cognitive performances, it may not prevent subsequent decline.


2020 ◽  
Vol 61 (10) ◽  
pp. 1308-1319
Author(s):  
Eileen E. Parks ◽  
Sreemathi Logan ◽  
Alexander Yeganeh ◽  
Julie A. Farley ◽  
Daniel B. Owen ◽  
...  

Cognitive decline with age is a harmful process that can reduce quality of life. Multiple factors have been established to contribute to cognitive decline, but the overall etiology remains unknown. Here, we hypothesized that cognitive dysfunction is mediated, in part, by increased levels of inflammatory cytokines that alter allopregnanolone (AlloP) levels, an important neurosteroid in the brain. We assessed the levels and regulation of AlloP and the effects of AlloP supplementation on cognitive function in 4-month-old and 24-month-old male C57BL/6 mice. With age, the expression of enzymes involved in the AlloP synthetic pathway was decreased and corticosterone (CORT) synthesis increased. Supplementation of AlloP improved cognitive function. Interestingly, interleukin 6 (IL-6) infusion in young animals significantly reduced the production of AlloP compared with controls. It is notable that inhibition of IL-6 with its natural inhibitor, soluble membrane glycoprotein 130, significantly improved spatial memory in aged mice. These findings were supported by in vitro experiments in primary murine astrocyte cultures, indicating that IL-6 decreases production of AlloP and increases CORT levels. Our results indicate that age-related increases in IL-6 levels reduce progesterone substrate availability, resulting in a decline in AlloP levels and an increase in CORT. Furthermore, our results indicate that AlloP is a critical link between inflammatory cytokines and the age-related decline in cognitive function.


2019 ◽  
Vol 14 (1) ◽  
pp. 121-134 ◽  
Author(s):  
Garazi Labayru ◽  
Jone Aliri ◽  
Miren Zulaica ◽  
Adolfo López de Munain ◽  
Andone Sistiaga

PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0204833 ◽  
Author(s):  
Asri Maharani ◽  
Piers Dawes ◽  
James Nazroo ◽  
Gindo Tampubolon ◽  
Neil Pendleton ◽  
...  

PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0208045 ◽  
Author(s):  
Asri Maharani ◽  
Piers Dawes ◽  
James Nazroo ◽  
Gindo Tampubolon ◽  
Neil Pendleton ◽  
...  

2019 ◽  
Vol 20 (3) ◽  
pp. 248-255 ◽  
Author(s):  
Sadanobu Ichii ◽  
Takumi Nakamura ◽  
Takeshi Kawarabayashi ◽  
Masamitsu Takatama ◽  
Tetsuya Ohgami ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2804
Author(s):  
Hitoshi Ozawa ◽  
Taiki Miyazawa ◽  
Teruo Miyazawa

Population aging has recently been an important issue as the number of elderly people is growing worldwide every year, and the extension of social security costs is financially costly. The increase in the number of elderly people with cognitive decline is a serious problem related to the aging of populations. Therefore, it is necessary to consider not only physical care but also cognitive patterns in the future care of older adults. Since food contains a variety of bioactive substances, dietary patterns may help improve age-related cognitive decline. However, the relationship between cognitive function and individual food components remains ambiguous as no clear efficacy or mechanism has been confirmed. Against this background, this review summarizes previous reports on the biological process of cognitive decline in the elderly and the relationship between individual compounds in foods and cognitive function, as well as the role of individual components of food in cognitive function, in the following order: lipids, carotenoids, vitamins, phenolic compounds, amino acids, peptides, and proteins. Based on the research presented in this review, a proper diet that preserves cognitive function has the potential to improve age-related cognitive decline, Alzheimer’s disease, and Parkinson’s disease. Hopefully, this review will help to trigger the development of new foods and technologies that improve aging and cognitive functions and extend the healthy life span.


Sign in / Sign up

Export Citation Format

Share Document