scholarly journals Evidence-Based Tools for Dietary Assessments in Nutrition Epidemiology Studies for Dementia Prevention

2022 ◽  
pp. 1-5
Author(s):  
K.A. Abbott ◽  
J.M. Posma ◽  
I. Garcia-Perez ◽  
C. Udeh-Momoh ◽  
S. Ahmadi-Abhari ◽  
...  
Keyword(s):  
Cognitive Aging ◽  
Measurement Errors ◽  
Disease Risk ◽  
Age Related ◽  
Dementia Prevention ◽  
Modifiable Factor ◽  
Disease Indicators ◽  
Epidemiology Studies ◽  
Nutrition Epidemiology ◽  
Age Related Cognitive Decline

Increasing evidence proposes diet as a notable modifiable factor and viable target for the reduction of Alzheimer’s Disease risk and age-related cognitive decline. However, assessment of dietary exposures is challenged by dietary capture methods that are prone to misreporting and measurement errors. The utility of -omics technologies for the evaluation of dietary exposures has the potential to improve reliability and offer new insights to pre-disease indicators and preventive targets in cognitive aging and dementia. In this review, we present a focused overview of metabolomics as a validation tool and framework for investigating the immediate or cumulative effects of diet on cognitive health.

Activity Engagement in Cognitive Aging: A Review of the Evidence

2013 ◽  
Vol 23 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Yvonne Rogalski ◽  
Muriel Quintana
Keyword(s):  
Older Adults ◽  
Cognitive Decline ◽  
Cognitive Aging ◽  
Social Activity ◽  
Current Evidence ◽  
Omega 3 ◽  
Neuroprotective Effects ◽  
Activity Engagement ◽  
Age Related ◽  
Age Related Cognitive Decline

The population of older adults is rapidly increasing, as is the number and type of products and interventions proposed to prevent or reduce the risk of age-related cognitive decline. Advocacy and prevention are part of the American Speech-Language-Hearing Association’s (ASHA’s) scope of practice documents, and speech-language pathologists must have basic awareness of the evidence contributing to healthy cognitive aging. In this article, we provide a brief overview outlining the evidence on activity engagement and its effects on cognition in older adults. We explore the current evidence around the activities of eating and drinking with a discussion on the potential benefits of omega-3 fatty acids, polyphenols, alcohol, and coffee. We investigate the evidence on the hypothesized neuroprotective effects of social activity, the evidence on computerized cognitive training, and the emerging behavioral and neuroimaging evidence on physical activity. We conclude that actively aging using a combination of several strategies may be our best line of defense against cognitive decline.

scholarly journals The TOMM40 ‘523’ polymorphism in disease risk and age of symptom onset in two independent cohorts of Parkinson’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Megan C. Bakeberg ◽  
Madison E. Hoes ◽  
Anastazja M. Gorecki ◽  
Frances Theunissen ◽  
Abigail L. Pfaff ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Symptom Onset ◽  
Disease Risk ◽  
Age Of Onset ◽  
Sequencing Analysis ◽  
Age Related ◽  
Australian Cohort ◽  
Progression Markers ◽  
Age Related Cognitive Decline

AbstractAbnormal mitochondrial function is a key process in the pathogenesis of Parkinson’s disease (PD). The central pore-forming protein TOM40 of the mitochondria is encoded by the translocase of outer mitochondrial membrane 40 homologue gene (TOMM40). The highly variant ‘523’ poly-T repeat is associated with age-related cognitive decline and age of onset in Alzheimer’s disease, but whether it plays a role in modifying the risk or clinical course of PD it yet to be elucidated. The TOMM40 ‘523’ allele length was determined in 634 people with PD and 422 healthy controls from an Australian cohort and the Parkinson’s Progression Markers Initiative (PPMI) cohort, using polymerase chain reaction or whole genome sequencing analysis. Genotype and allele frequencies of TOMM40 ‘523’ and APOE ε did not differ significantly between the cohorts. Analyses revealed TOMM40 ‘523’ allele groups were not associated with disease risk, while considering APOE ε genotype. Regression analyses revealed the TOMM40 S/S genotype was associated with a significantly later age of symptom onset in the PPMI PD cohort, but not after correction for covariates, or in the Australian cohort. Whilst variation in the TOMM40 ‘523’ polymorphism was not associated with PD risk, the possibility that it may be a modifying factor for age of symptom onset warrants further investigation in other PD populations.

scholarly journals Gene Expression Profile in Different Age Groups and Its Association with Cognitive Function in Healthy Malay Adults in Malaysia

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1611
Author(s):  
Nur Fathiah Abdul Abdul Sani ◽  
Ahmad Imran Zaydi Amir Amir Hamzah ◽  
Zulzikry Hafiz Abu Abu Bakar ◽  
Yasmin Anum Mohd Mohd Yusof ◽  
Suzana Makpol ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cognitive Decline ◽  
Cognitive Aging ◽  
Successful Aging ◽  
Expression Patterns ◽  
Age Groups ◽  
Genetic Network ◽  
Cross Sectional ◽  
Age Related ◽  
Age Related Cognitive Decline

The mechanism of cognitive aging at the molecular level is complex and not well understood. Growing evidence suggests that cognitive differences might also be caused by ethnicity. Thus, this study aims to determine the gene expression changes associated with age-related cognitive decline among Malay adults in Malaysia. A cross-sectional study was conducted on 160 healthy Malay subjects, aged between 28 and 79, and recruited around Selangor and Klang Valley, Malaysia. Gene expression analysis was performed using a HumanHT-12v4.0 Expression BeadChip microarray kit. The top 20 differentially expressed genes at p < 0.05 and fold change (FC) = 1.2 showed that PAFAH1B3, HIST1H1E, KCNA3, TM7SF2, RGS1, and TGFBRAP1 were regulated with increased age. The gene set analysis suggests that the Malay adult’s susceptibility to developing age-related cognitive decline might be due to the changes in gene expression patterns associated with inflammation, signal transduction, and metabolic pathway in the genetic network. It may, perhaps, have important implications for finding a biomarker for cognitive decline and offer molecular targets to achieve successful aging, mainly in the Malay population in Malaysia.

scholarly journals INTEREST GROUP SESSION—SLEEP, CIRCADIAN RHYTHMS AND AGING INTEREST GROUP: SLEEP, PHYSICAL ACTIVITY, AND BRAIN AGING

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S402-S403
Author(s):  
Christopher N Kaufmann ◽  
Katie L Stone
Keyword(s):  
Circadian Rhythms ◽  
Sleep Disturbance ◽  
Interest Group ◽  
Cognitive Aging ◽  
Brain Aging ◽  
Disease Risk ◽  
Activity Patterns ◽  
Time Of Day ◽  
Daytime Activity ◽  
Dementia Prevention

Abstract As the US population ages, the prevalence of Alzheimer’s Disease (AD) and related dementias is expected to increase, making dementia prevention efforts a major public health priority. Impaired sleep and circadian rhythms, along with other lifestyle factors, have emerged as important modifiable disease risk factors—recent studies demonstrate the importance of sleep in preventing the development of key biomarkers for AD/dementia pathology. In this symposium, we will highlight findings on the associations of sleep, circadian rhythm disruptions, and daytime activity patterns on development of cognitive decline and dementia, exploring not only the mechanisms driving these associations, but the potential impact of sleep and lifestyle interventions in promoting healthy brain aging. The symposium consists of four presentations which use data from large national cohort studies. First, we will present analyses on patterns of 24-hour (circadian) activity rhythms (e.g., usual time of day for peak activity, regularity of circadian patterns) and incident dementia risk. The second presentation will present findings pertaining to understanding the link between sleep disturbance and inflammation (a substantial contributor to cognitive aging). The third will examine whether detailed daytime activity patterns associate with imaging-based brain volumes, independent of sleep disturbance. The final presentation will explore whether initiation of sleep disorder treatments may have the potential to change trajectories of cognitive performance as individuals age. Overall, the symposium will highlight the importance of sleep and activity patterns to brain health and stimulate discussion about improving sleep and circadian disruption as a target for dementia prevention efforts.

Do Professors Better Maintain Cognitive Functioning in Older Age?

GeroPsych ◽  
2019 ◽  
Vol 32 (1) ◽  
pp. 5-17
Author(s):  
Damaris Aschwanden ◽  
Vera Schumacher ◽  
Kathrin Zimmermann ◽  
Christina Werner ◽  
Mathias Allemand ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Performance ◽  
Cognitive Aging ◽  
Protective Factor ◽  
Perceptual Speed ◽  
Highly Educated ◽  
Intellectual Engagement ◽  
Age Related ◽  
Average Education ◽  
Age Related Cognitive Decline

Abstract. Research on cognitive aging demonstrates age-related cognitive decline. Education is a protective factor against cognitive decline, but few studies have examined the cognitive development of highly educated individuals. This study compared the cognitive performance and intellectual engagement of retired professors ( N = 47, Mage = 72.9) and individuals with average education ( N = 236, Mage = 72.7) over 5 years. Although the highly educated sample showed better performance in perceptual speed and working memory, cognitive performance was rather stable over time in both samples. Interestingly, high intellectual engagement enabled individuals with average education to keep up with the performance of the highly educated sample on perceptual speed. These findings raise the question whether intellectual engagement is more beneficial than years of education in perceptual speed.

scholarly journals Preserved wake-dependent cortical excitability dynamics predict cognitive fitness beyond age-related brain alterations

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Maxime Van Egroo ◽  
Justinas Narbutas ◽  
Daphne Chylinski ◽  
Pamela Villar González ◽  
Pouya Ghaemmaghami ◽  
...  
Keyword(s):  
Cognitive Aging ◽  
Structural Integrity ◽  
Cortical Excitability ◽  
Older Individuals ◽  
Cortical Function ◽  
Structural Modifications ◽  
Age Related ◽  
Age Related Cognitive Decline ◽  
Positive Factor ◽  
Sensitive Marker

AbstractAge-related cognitive decline arises from alterations in brain structure as well as in sleep-wake regulation. Here, we investigated whether preserved wake-dependent regulation of cortical function could represent a positive factor for cognitive fitness in aging. We quantified cortical excitability dynamics during prolonged wakefulness as a sensitive marker of age-related alteration in sleep-wake regulation in 60 healthy older individuals (50–69 y; 42 women). Brain structural integrity was assessed with amyloid-beta- and tau-PET, and with MRI. Participants’ cognition was investigated using an extensive neuropsychological task battery. We show that individuals with preserved wake-dependent cortical excitability dynamics exhibit better cognitive performance, particularly in the executive domain which is essential to successful cognitive aging. Critically, this association remained significant after accounting for brain structural integrity measures. Preserved dynamics of basic brain function during wakefulness could therefore be essential to cognitive fitness in aging, independently from age-related brain structural modifications that can ultimately lead to dementia.

Exercise and dementia prevention

2020 ◽  
Vol 20 (3) ◽  
pp. 234-240 ◽  
Author(s):  
Jane Alty ◽  
Maree Farrow ◽  
Katherine Lawler
Keyword(s):  
Risk Factors ◽  
Physical Inactivity ◽  
Lifestyle Changes ◽  
Current Evidence ◽  
Prevention Strategies ◽  
Neuroprotective Drugs ◽  
Age Related ◽  
Dementia Risk ◽  
Dementia Prevention ◽  
Age Related Cognitive Decline

Ageing, genetic, medical and lifestyle factors contribute to the risk of Alzheimer’s disease and other dementias. Around a third of dementia cases are attributable to modifiable risk factors such as physical inactivity, smoking and hypertension. With the rising prevalence and lack of neuroprotective drugs, there is renewed focus on dementia prevention strategies across the lifespan. Neurologists encounter many people with risk factors for dementia and are frequently asked whether lifestyle changes may help. Exercise has emerged as a key intervention for influencing cognition positively, including reducing the risk of age-related cognitive decline and dementia. This article focuses on the current evidence for physical inactivity as a modifiable dementia risk factor and aims to support neurologists when discussing risk reduction.

scholarly journals The TOMM40 ‘523’ polymorphism in disease risk and age of symptom onset in two independent cohorts of Parkinson’s disease.

2020 ◽  
Author(s):  
Megan Bakeberg ◽  
Madison Hoes ◽  
Anastazja Gorecki ◽  
Frances Theunissen ◽  
Abigail Pfaff ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Symptom Onset ◽  
Disease Risk ◽  
Age Of Onset ◽  
Sequencing Analysis ◽  
Age Related ◽  
Australian Cohort ◽  
Progression Markers ◽  
Age Related Cognitive Decline

Abstract Abnormal mitochondrial function is a key process in the pathogenesis of Parkinson’s disease (PD). The central pore-forming protein TOM40 of the mitochondria is encoded by the translocase of outer mitochondrial membrane 40 homologue gene (TOMM40). The highly variant poly-T repeat is associated with age-related cognitive decline and age of onset in Alzheimer’s disease, but whether it plays a role in modifying the risk or clinical course of PD it yet to be elucidated. The TOMM40 allele length was determined in 634 people with PD and 422 healthy controls from an Australian cohort and the Parkinson’s Progression Markers Initiative (PPMI) cohort, using polymerase chain reaction or whole genome sequencing analysis. Genotype and allele frequencies of TOMM40 and APOE ε did not differ significantly between the cohorts. Analyses revealed TOMM40 groups were not associated with disease risk, while considering APOE ε genotype. Regression analyses revealed the TOMM40 S/S genotype was associated with a significantly later age of symptom onset in the PPMI PD cohort, but not in the Australian cohort. Variation in the TOMM40 structural variant was not associated with PD risk, but may be a modifying factor for age of symptom onset in some PD populations, warranting further investigation.

scholarly journals Preserved wake-dependent cortical excitability dynamics predict cognitive fitness beyond age-related brain alterations

2019 ◽  
Author(s):  
Maxime Van Egroo ◽  
Justinas Narbutas ◽  
Daphne Chylinski ◽  
Pamela Villar González ◽  
Pouya Ghaemmaghami ◽  
...  
Keyword(s):  
Cognitive Aging ◽  
Structural Integrity ◽  
Cortical Excitability ◽  
Older Individuals ◽  
Cortical Function ◽  
Structural Modifications ◽  
Age Related ◽  
Age Related Cognitive Decline ◽  
Positive Factor ◽  
Sensitive Marker

AbstractAge-related cognitive decline arises from alterations in brain integrity as well as in sleep-wake regulation. Here, we investigated whether preserved sleep-wake regulation of cortical function during wakefulness could represent a positive factor for cognitive fitness in aging, independently of early age-related changes in brain structure. We quantified cortical excitability dynamics during prolonged wakefulness as a sensitive marker of age-related alteration in sleep-wake regulation in 60 healthy older individuals (50-69y; 42 women). Brain structural integrity was assessed with amyloid-beta- and tau-PET, and with MRI. Participants’ cognition was extensively investigated. We show that individuals with preserved cortical excitability dynamics exhibit better cognitive performance, particularly in the executive domain, which is essential to successful cognitive aging. Critically, this association remained significant after accounting for brain integrity measures. Preserved dynamics of basic brain function during wakefulness could be essential to cognitive fitness in aging, independently from age-related brain structural modifications that can ultimately lead to dementia.

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