| 61. |
- Griffiths, William J., et al.
(författare)
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The Cerebrospinal Fluid Profile of Cholesterol Metabolites in Parkinson’s Disease and Their Association With Disease State and Clinical Features
- 2021
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media S.A.. - 1663-4365 .- 1663-4365. ; 13
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Tidskriftsartikel (refereegranskat)abstract
- Disordered cholesterol metabolism is linked to neurodegeneration. In this study we investigated the profile of cholesterol metabolites found in the cerebrospinal fluid (CSF) of Parkinson’s disease (PD) patients. When adjustments were made for confounding variables of age and sex, 7α,(25R)26-dihydroxycholesterol and a second oxysterol 7α,x,y-trihydroxycholest-4-en-3-one (7α,x,y-triHCO), whose exact structure is unknown, were found to be significantly elevated in PD CSF. The likely location of the additional hydroxy groups on the second oxysterol are on the sterol side-chain. We found that CSF 7α-hydroxycholesterol levels correlated positively with depression in PD patients, while two presumptively identified cholestenoic acids correlated negatively with depression.
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| 62. |
- Gronholm-Nyman, Petra, et al.
(författare)
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Limited Effects of Set Shifting Training in Healthy Older Adults
- 2017
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media S.A.. - 1663-4365 .- 1663-4365. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Our ability to flexibly shift between tasks or task sets declines in older age. As this decline may have adverse effects on everyday life of elderly people, it is of interest to study whether set shifting ability can be trained, and if training effects generalize to other cognitive tasks. Here, we report a randomized controlled trial where healthy older adults trained set shifting with three different set shifting tasks. The training group (n = 17) performed adaptive set shifting training for 5 weeks with three training sessions a week (45 min/session), while the active control group (n = 16) played three different computer games for the same period. Both groups underwent extensive pre-and post-testing and a 1-year follow-up. Compared to the controls, the training group showed significant improvements on the trained tasks. Evidence for near transfer in the training group was very limited, as it was seen only on overall accuracy on an untrained computerized set shifting task. No far transfer to other cognitive functions was observed. One year later, the training group was still better on the trained tasks but the single near transfer effect had vanished. The results suggest that computerized set shifting training in the elderly shows long-lasting effects on the trained tasks but very little benefit in terms of generalization.
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| 63. |
- Gudberg, Christel, et al.
(författare)
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Individual differences in slow wave sleep architecture relate to variation in white matter microstructure across adulthood
- 2022
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media S.A.. - 1663-4365 .- 1663-4365. ; 14
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Tidskriftsartikel (refereegranskat)abstract
- Sleep plays a key role in supporting brain function and resilience to brain decline. It is well known that sleep changes substantially with aging and that aging is associated with deterioration of brain structure. In this study, we sought to characterize the relationship between slow wave slope (SWslope)—a key marker of sleep architecture and an indirect proxy of sleep quality—and microstructure of white matter pathways in healthy adults with no sleep complaints. Participants were 12 young (24–27 years) and 12 older (50–79 years) adults. Sleep was assessed with nocturnal electroencephalography (EEG) and the Pittsburgh Sleep Quality Index (PSQI). White matter integrity was assessed using tract-based spatial statistics (TBSS) on tensor-based metrics such as Fractional Anisotropy (FA) and Mean Diffusivity (MD). Global PSQI score did not differ between younger (n = 11) and older (n = 11) adults (U = 50, p = 0.505), but EEG revealed that younger adults had a steeper SWslope at both frontal electrode sites (F3: U = 2, p < 0.001, F4: U = 4, p < 0.001, n = 12 younger, 10 older). There were widespread correlations between various diffusion tensor-based metrics of white matter integrity and sleep SWslope, over and above effects of age (n = 11 younger, 9 older). This was particularly evident for the corpus callosum, corona radiata, superior longitudinal fasciculus, internal and external capsule. This indicates that reduced sleep slow waves may be associated with widespread white matter deterioration. Future studies should investigate whether interventions targeted at improving sleep architecture also impact on decline in white matter microstructure in older adults.
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| 64. |
- Haller, Sven, et al.
(författare)
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Automatic MRI volumetry in asymptomatic cases at risk for normal pressure hydrocephalus
- 2023
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media S.A.. - 1663-4365 .- 1663-4365. ; 15
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Tidskriftsartikel (refereegranskat)abstract
- The occurrence of significant Alzheimer's disease (AD) pathology was described in approximately 30% of normal pressure hydrocephalus (NPH) cases, leading to the distinction between neurodegenerative and idiopathic forms of this disorder. Whether or not there is a specific MRI signature of NPH remains a matter of debate. The present study focuses on asymptomatic cases at risk for NPH as defined with automatic machine learning tools and combines automatic MRI assessment of cortical and white matter volumetry, risk of AD (AD-RAI), and brain age gap estimation (BrainAge). Our hypothesis was that brain aging and AD process-independent volumetric changes occur in asymptomatic NPH-positive cases. We explored the volumetric changes in normal aging-sensitive (entorhinal cortex and parahippocampal gyrus/PHG) and AD-signature areas (hippocampus), four control cortical areas (frontal, parietal, occipital, and temporal), and cerebral and cerebellar white matter in 30 asymptomatic cases at risk for NPH (NPH probability >30) compared to 30 NPH-negative cases (NPH probability <5) with preserved cognition. In univariate regression models, NPH positivity was associated with decreased volumes in the hippocampus, parahippocampal gyrus (PHG), and entorhinal cortex bilaterally. The strongest negative association was found in the left hippocampus that persisted when adjusting for AD-RAI and Brain Age values. A combined model including the three parameters explained 36.5% of the variance, left hippocampal volumes, and BrainAge values, which remained independent predictors of the NPH status. Bilateral PHG and entorhinal cortex volumes were negatively associated with NPH-positive status in univariate models but this relationship did not persist when adjusting for BrainAge, the latter remaining the only predictor of the NPH status. We also found a negative association between bilateral cerebral and cerebellar white matter volumes and NPH status that persisted after controlling for AD-RAI or Brain Age values, explaining between 50 and 65% of its variance. These observations support the idea that in cases at risk for NPH, as defined by support vector machine assessment of NPH-related MRI markers, brain aging-related and brain aging and AD-independent volumetric changes coexist. The latter concerns volume loss in restricted hippocampal and white matter areas that could be considered as the MRI signature of idiopathic forms of NPH.
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| 65. |
- Hassing, Linda, 1967
(författare)
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Light alcohol consumption does not protect cognitive function: A longitudinal prospective study
- 2018
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media SA. - 1663-4365. ; 10:March
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Tidskriftsartikel (refereegranskat)abstract
- Studies show that light to moderate alcohol consumption is related to better health and higher cognitive performance. However, it has been suggested that this association is caused by a systematic bias in the control group as many people abstain from drinking or quit because of health issues. Therefore, the group of non-drinkers is biased towards poor health and may not be suitable as a control group. The present study examined the effect of alcohol on cognitive performance while addressing this bias by excluding the non-drinkers. Thus, instead of comparing different levels of alcohol consumption to a non-drinking control group, a dose-response association was calculated between all levels of alcohol intake and cognitive performance. The study used information from a sample of people in the Swedish Twin Registry, who in their midlife (1967) participated in a survey on alcohol intake and 25 years later participated in a longitudinal study on cognitive aging (N = 486). The cognitive aging study took place on five occasions, at 2-year intervals, and included the Mini Mental State Examination (MMSE), tests of episodic memory, semantic memory and spatial ability. The association between midlife alcohol consumption and later cognitive performance was analyzed using growth curve models, adjusting for background variables. The findings showed that there was a significant negative dose-response association between alcohol intake in midlife and the MMSE, and the tests of episodic memory, such that higher intake in midlife was related to lower performance in old age. The associations between alcohol and semantic memory, and spatial ability respectively, were not significant. In contrast to findings from other studies, which show that low to moderate alcohol intake promotes cognitive function, the current study showed that alcohol intake was related to lower cognitive performance in a dose-response manner, even at low levels. The results from this study indicate that the observed benefits of moderate alcohol intake for cognitive function reported by others might be solely due to comparisons to an inappropriate control group, a group that is biased towards poor health. Hence, it is concluded that light alcohol intake may not protect cognitive function. © 2018 Hassing.
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| 66. |
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| 67. |
- Hedner, Margareta, et al.
(författare)
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Age-Related Olfactory Decline is Associated with the BDNF Val66met Polymorphism : Evidence from a Population-Based Study
- 2010
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media SA. - 1663-4365. ; 2:7, s. 24-
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Tidskriftsartikel (refereegranskat)abstract
- The present study investigates the effect of the brain-derived neurotrophic factor (BDNF) val66met polymorphism on change in olfactory function in a large scale, longitudinal population-based sample (n = 836). The subjects were tested on a 13 item force-choice odor identification test on two test occasions over a 5-year-interval. Sex, education, health-related factors, and semantic ability were controlled for in the statistical analyses. Results showed an interaction effect of age and BDNF val66met on olfactory change, such that the magnitude of olfactory decline in the older age cohort (70–90years old at baseline) was larger for the val homozygote carriers than for the met carriers. The older met carriers did not display larger age-related decline in olfactory function compared to the younger group. The BDNF val66met polymorphism did not affect the rate of decline in the younger age cohort (45–65years). The findings are discussed in the light of the proposed roles of BDNF in neural development and maintenance.
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| 68. |
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| 69. |
- Herrmann, François R, et al.
(författare)
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Gray Matter Densities in Limbic Areas and APOE4 Independently Predict Cognitive Decline in Normal Brain Aging
- 2019
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media SA. - 1663-4365 .- 1663-4365. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- Cross-sectional magnetic resonance imaging (MRI) studies reported significant associations between gray matter (GM) density changes in various limbic and neocortical areas and worst cognitive performances in elderly controls. Longitudinal studies in this field remain scarce and led to conflicting data. We report a clinico-radiological investigation of 380 cognitively preserved individuals who undergo neuropsychological assessment at baseline and after 18 months. All cases were assessed using a continuous cognitive score taking into account the global evolution of neuropsychological performances. The vast majority of Mini Mental State Examination (MMSE) 29 and 30 cases showed equal or worst performance at follow-up due to a ceiling effect. GM densities, white matter hyperintensities and arterial spin labeling (ASL) values were assessed in the hippocampus, amygdala, mesial temporal and parietal cortex at inclusion using 3 Tesla MRI Scans. Florbetapir positron emission tomography (PET) amyloid was available in a representative subsample of 64 cases. Regional amyloid uptake ratios (SUVr), mean cortical SUVr values (mcSUVr) and corresponding z-scores were calculated. Linear regression models were built to explore the association between the continuous cognitive score and imaging variables. The presence of an APOE-epsilon 4 allele was negatively related to the continuous cognitive score. Among the areas studied, significant associations were found between GM densities in the hippocampus and amygdala but not mesial temporal and parietal areas and continuous cognitive score. Neither ASL values, Fazekas score nor mean and regional PET amyloid load was related to the cognitive score. In multivariate models, the presence of APOE-epsilon 4 allele and GM densities in the hippocampus and amygdala were independently associated with worst cognitive evolution at follow-up. Our data support the idea that early GM damage in the hippocampus and amygdala occur long before the emergence of the very first signs of cognitive failure in brain aging.
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| 70. |
- Holmberg, Johan K, et al.
(författare)
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Laminin α2 Chain-Deficiency is Associated with microRNA Deregulation in Skeletal Muscle and Plasma.
- 2014
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Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media SA. - 1663-4365. ; 6:Jul 3
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Tidskriftsartikel (refereegranskat)abstract
- microRNAs (miRNAs) are widespread regulators of gene expression, but little is known of their potential roles in congenital muscular dystrophy type 1A (MDC1A). MDC1A is a severe form of muscular dystrophy caused by mutations in the gene encoding laminin α2 chain. To gain insight into the pathophysiological roles of miRNAs associated with MDC1A pathology, laminin α2 chain-deficient mice were evaluated by quantitative PCR. We demonstrate that expression of muscle-specific miR-1, miR-133a, and miR-206 is deregulated in laminin α2 chain-deficient muscle. Furthermore, expression of miR-223 and miR-21, associated with immune cell infiltration and fibrosis, respectively, is altered. Finally, we show that plasma levels of muscle-specific miRNAs are markedly elevated in laminin α2 chain-deficient mice and partially normalized in response to proteasome inhibition therapy. Altogether, our data suggest important roles for miRNAs in MDC1A pathology and we propose plasma levels of muscle-specific miRNAs as promising biomarkers for the progression of MDC1A.
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