ORCID Profile
0000-0001-5476-9526
Current Organisation
University of Queensland
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Publisher: American Psychological Association (APA)
Date: 2015
DOI: 10.1037/NEU0000249
Abstract: Increasing an in idual's level of cognitive reserve (CR) has been suggested as a nonpharmacological approach to reducing the risk for Alzheimer's disease. We examined changes in CR in older adults participating over 4 years in the Tasmanian Healthy Brain Project. A s le of 459 healthy older adults between 50 and 79 years of age underwent a comprehensive annual assessment of current CR, neuropsychological function, and psychosocial factors over a 4-year period. The intervention group of 359 older adults (M = 59.61 years, SD = 6.67) having completed a minimum of 12 months part-time university study were compared against a control reference group of 100 adults (M = 62.49 years, SD = 6.24) who did not engage in further education. Growth mixture modeling demonstrated that 44.3% of the control s le showed no change in CR, whereas 92.5% of the further education participants displayed a significant linear increase in CR over the 4 years of the study. These results indicate that older adults engaging in high-level mental stimulation display an increase in CR over a 4-year period. Increasing mental activity in older adulthood may be a viable strategy to improve cognitive function and offset cognitive decline associated with normal aging. (PsycINFO Database Record
Publisher: Elsevier BV
Date: 2021
Publisher: Wiley
Date: 12-2021
DOI: 10.1002/AGM2.12187
Abstract: Frailty is an established risk factor for cognitive decline and Alzheimer's disease. Few studies have examined the longitudinal relationship between frailty and cognition. Participants of Rush Memory and Aging project ( n = 625, 67.5% female, 83.2 ± 5.9 years at baseline) underwent annual clinical evaluations (average follow‐up 5.6 ± 3.7 years) followed by neuropathologic assessment after death. A frailty index was calculated from 41 health variables at each evaluation. Clinical diagnosis of MCI and/or dementia was ascertained by clinical data review (blinded to neuropathological data) after death. Age, sex, education, and neuropathological burden (10‐item index) were evaluated as covariates. Frailty trajectories were calculated using a mixed effects model. At baseline the mean frailty index = 0.24 ± 0.12 and increased at rate of 0.026 or ~1 deficit per year. At death, 27.7% of the s le had MCI, and 38.6% had dementia. Frailty trajectories were significantly steeper among those in iduals who were ultimately diagnosed as clinically impaired prior to death, even after controlling for age, sex, education, and neuropathological index. Findings suggest a strong link between health status (frailty index) and dementia, even after considering neuropathology. Frailty trajectories were associated with risk for MCI and dementia, underscoring the importance of addressing frailty to manage dementia risk.
Publisher: MDPI AG
Date: 25-03-2020
Abstract: Brain-derived neurotropic factor (BDNF) is an abundant and multi-function neurotrophin in the brain. It is released following neuronal activity and is believed to be particularly important in strengthening neural networks. A common variation in the BDNF gene, a valine to methionine substitution at codon 66 (Val66Met), has been linked to differential expression of BDNF associated with experience-dependent plasticity. The Met allele has been associated with reduced production of BDNF following neuronal stimulation, which suggests a potential role of this variation with respect to how the nervous system may respond to challenges, such as brain ageing and related neurodegenerative conditions (e.g., dementia and Alzheimer’s disease). The current review examines the potential of the BDNF Val66Met variation to modulate an in idual’s susceptibility and trajectory through cognitive changes associated with ageing and dementia. On balance, research to date indicates that the BDNF Met allele at this codon is potentially associated with a detrimental influence on the level of cognitive functioning in older adults and may also impart increased risk of progression to dementia. Furthermore, recent studies also show that this genetic variation may modulate an in idual’s response to interventions targeted at building cognitive resilience to conditions that cause dementia.
Publisher: Springer Science and Business Media LLC
Date: 06-06-2017
DOI: 10.1038/TP.2017.107
Publisher: Wiley
Date: 15-05-2017
Publisher: Wiley
Date: 22-09-2023
DOI: 10.1111/ENE.16072
Publisher: Cambridge University Press (CUP)
Date: 08-2021
Publisher: BMJ
Date: 13-11-2020
Abstract: To determine whether health-deficit accumulation is associated with the risks of mild cognitive impairment (MCI) and dementia independently of APOE genotype. A frailty index was calculated using the deficit-accumulation approach in participants aged 50 years and older from the National Alzheimer’s Coordinating Center. Cognitive status was determined by clinical evaluation. Using multistate transition models, we assessed the extent to which an increasing degree of frailty affected the probabilities of transitioning between not cognitively impaired (NCI), MCI, and dementia. Participants (n=14 490) had a mean age of 72.2 years (SD=8.9 years range=50–103 years). Among those NCI at baseline (n=9773), each 0.1 increment increase in the frailty index was associated with a higher risk of developing MCI and a higher risk of progressing to dementia. Among those with MCI at baseline (n=4717), higher frailty was associated with a higher risk of progressing to dementia, a lower probability of being reclassified as NCI, and a higher likelihood of returning to MCI in those that were reclassified as NCI. These risk effects were present and similar in both carriers and non-carriers of the APOE ε4 allele. Among older Americans, health-deficit accumulation affects the likelihood of progressive cognitive impairment and the likelihood of cognitive improvement independently of a strong genetic risk factor for dementia. Frailty represents an important risk factor for cognitive dysfunction and a marker of potential prognostic value.
Publisher: Springer Science and Business Media LLC
Date: 15-11-2017
DOI: 10.1038/S41539-017-0014-5
Abstract: Although predictors of academic success have been identified in young adults, such predictors are unlikely to translate directly to an older student population, where such information is scarce. The current study aimed to examine cognitive, psychosocial, lifetime, and genetic predictors of university-level academic performance in older adults (50–79 years old). Participants were mostly female (71%) and had a greater than high school education level ( M = 14.06 years, SD = 2.76), on average. Two multiple linear regression analyses were conducted. The first examined all potential predictors of grade point average (GPA) in the subset of participants who had volunteered s les for genetic analysis ( N = 181). Significant predictors of GPA were then re-examined in a second multiple linear regression using the full s le ( N = 329). Our data show that the cognitive domains of episodic memory and language processing, in conjunction with midlife engagement in cognitively stimulating activities, have a role in predicting academic performance as measured by GPA in the first year of study. In contrast, it was determined that age, IQ, gender, working memory, psychosocial factors, and common brain gene polymorphisms linked to brain function, plasticity and degeneration ( APOE , BDNF , COMT , KIBRA, SERT ) did not influence academic performance. These findings demonstrate that ageing does not impede academic achievement, and that discrete cognitive skills as well as lifetime engagement in cognitively stimulating activities can promote academic success in older adults.
Publisher: BMJ
Date: 21-12-2021
Abstract: To optimise dementia prevention strategies, we must understand the complex relationships between lifestyle behaviours, frailty and genetics. We explored relationships between frailty index, healthy lifestyle and polygenic risk scores (all assessed at study entry) and incident all-cause dementia as recorded on hospital admission records and death register data. The analytical s le had a mean age of 64.1 years at baseline (SD=2.9) and 53% were women. Incident dementia was detected in 1762 participants (median follow-up time=8.0 years). High frailty was associated with increased dementia risk independently of genetic risk (HR 3.68, 95% CI 3.11 to 4.35). Frailty mediated 44% of the relationship between healthy lifestyle behaviours and dementia risk (indirect effect HR 0.95, 95% CI 0.95 to 0.96). Participants at high genetic risk and with high frailty had 5.8 times greater risk of incident dementia compared with those at low genetic risk and with low frailty (HR 5.81, 95% CI 4.01 to 8.42). Higher genetic risk was most influential in those with low frailty (HR 1.31, 95% CI 1.22 to 1.40) but not influential in those with high frailty (HR 1.09, 95% CI 0.92 to 1.28). Frailty is strongly associated with dementia risk and affects the risk attributable to genetic factors. Frailty should be considered an important modifiable risk factor for dementia and a target for dementia prevention strategies, even among people at high genetic risk.
Publisher: SAGE Publications
Date: 02-01-2017
Abstract: Cognitive reserve (CR) is a theoretical construct describing the underlying cognitive capacity of an in idual that confers differential levels of resistance to, and recovery from, brain injuries of various types. To date, estimates of an in idual's level of CR have been based on single proxy measures that are retrospective and static in nature. To develop a measure of dynamic change in CR across a lifetime, we previously identified a latent factor, derived from an exploratory factor analysis of a large s le of healthy older adults, as current CR (cCR). In the present study, we examined the longitudinal results of a s le of 272 older adults enrolled in the Tasmanian Healthy Brain Project. Using results from 12-month and 24-month reassessments, we examined the longitudinal validity of the cCR factor using confirmatory factor analyses. The results of these analyses indicate that the cCR factor structure is longitudinally stable. These results, in conjunction with recent results from our group demonstrating dynamic increases in cCR over time in older adults undertaking further education, lend weight to this cCR measure being a valid estimate of dynamic change in CR over time.
Publisher: Elsevier BV
Date: 11-2020
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 25-06-2002
DOI: 10.1212/WNL.0000000000010146
Abstract: To quantify the associations of peripapillary retinal nerve fiber layer (pRNFL) thickness and macular ganglion cell layer (mGCL) volume with cognitive functioning and to investigate how demographic and vascular health factors affect these associations in a population-based s le of adults. The s le included the first 3,000 participants (age range 30–95 years) of the Rhineland Study (recruited from March 2016 to December 2018) who underwent spectral-domain optical coherence tomography and cognitive assessment at 1 of 2 identical study centers in Bonn, Germany. We used multiple linear regression models to examine the relationships between retinal layer measurements and cognitive functioning after adjustment for confounders, and we examined the moderating effects of demographic and vascular health factors. The analytical s le included 2,483 participants who were 54.3 years old (SD 13.8 years) on average. After full adjustment, each 1-SD decrease in mGCL volume was associated with a greater decrease in global function than that of pRNFL thickness (β = −0.048 [95% confidence interval (CI) −0.077 to −0.018] vs β = −0.021 [95% CI −0.049 to 0.007]). These relationships increased in strength with advancing age, were stronger in participants with hypertension, and were reversed in current smokers relative to nonsmokers. mGCL volume is more strongly related to adult cognitive functioning than pRNFL thickness, making it a better potential biomarker of neurodegeneration. Age and vascular health factors play important roles in determining the strength and direction of this association.
Publisher: Frontiers Media SA
Date: 25-08-190728635
Publisher: Wiley
Date: 21-03-2021
DOI: 10.1002/ANA.26064
Abstract: Risk factors for developing dementia from mild cognitive impairment (MCI) probably differ between MCI subtypes. We investigated how frailty relates to dementia risk in amnestic MCI (a‐MCI n = 2,799) and non‐amnestic MCI (na‐MCI n = 629) in the National Alzheimer's Coordinating Center database. Although higher frailty increased dementia risk for people with either a‐MCI or na‐MCI, the larger risk was in na‐MCI (interaction hazard ratio = 1.35 [95% confidence interval = 1.15–1.59], p 0.001). Even after the onset of clinically significant cognitive impairment, poor general health, quantified by a high degree of frailty, is a significant risk for dementia. ANN NEUROL 2021 :1221–1225
Publisher: SERDI
Date: 2019
Abstract: In 358 participants of the Tasmanian Healthy Brain Project, we quantified the cognitive consequences of engaging in varying loads of university-level education in later life, and investigated whether or not BDNF Val66Met affected outcomes. Assessment of neuropsychological, health, and psychosocial function was undertaken at baseline, 12-month, and 24-month follow-up. Education load was positively associated with change in language processing performance, but this effect did not reach statistical significance (P = 0.064). The BDNF Val66Met polymorphism significantly moderated the extent to which education load was associated with improved language processing (P = 0.026), with education load having a significant positive relationship with cognitive change in BDNF Met carriers but not in BDNF Val homozygotes. In older adults who carry BDNF Met, engaging in university-level education improves language processing performance in a load-dependent manner.
Location: Germany
Start Date: 2016
End Date: 2017
Funder: Dementia Collaborative Research Centre
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