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  • Allard, Per, et al. (författare)
  • Age-correlated loss of dopamine uptake sites labeled with [3H]GBR-12935 in human putamen.
  • 1989
  • Ingår i: Neurobiology of Aging. - 0197-4580 .- 1558-1497. ; 10:6, s. 661-4
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects of age (19-100 years) upon dopamine uptake sites labeled with [3H]GBR-12935 in human postmortem putamen from 20 individuals were studied. There was a 70% decrease in binding density (Bmax) over the adult age range. No significant changes in binding affinity (Kd) were detected, the mean Kd being 1.0 +/- 0.2 nM (mean +/- S.E.M.). Nor were there any changes in binding related to the postmortem delay. Based on the findings that [3H]GBR-12935 labels the uptake site for dopamine, it is suggested that the age-related loss of [3H]GBR-12935 binding in human putamen reflects a degeneration of dopamine neurites.
  • Allison, Samantha L, et al. (författare)
  • Neurodegeneration, Alzheimer's disease biomarkers, and longitudinal verbal learning and memory performance in late middle age.
  • 2021
  • Ingår i: Neurobiology of aging. - 1558-1497. ; 102, s. 151-160
  • Tidskriftsartikel (refereegranskat)abstract
    • This study examined the effect of neurodegeneration, and its interaction with Alzheimer's disease (AD) cerebrospinal fluid biomarkers, on longitudinal verbal learning and memory performance in cognitively unimpaired (CU) late middle-aged adults. Three hundred and forty-two CU adults (cognitive baseline mean age = 58.4), with cerebrospinal fluid and structural MRI, completed 2-10 (median = 5) cognitive assessments. Learning and memory were assessed using the Rey Auditory Verbal Learning Test (RAVLT). We used sequential comparison of nested linear mixed effects models to analyze the data. Model selection preserved a significant ptau181/Aβ42 × global atrophy × age interaction; individuals with less global atrophy and lower ptau181/Aβ42 levels had less learning and delayed recall decline than individuals with more global atrophy and/or higher levels of ptau181/Aβ42. The hippocampal volume × age × ptau181/Aβ42 interaction was not significant. Findings suggest that in a sample of CU late middle-aged adults, individuals with AD biomarkers, global atrophy, or both evidence greater verbal learning and memory decline than individuals without either risk factor.
  • Almkvist, Ove, et al. (författare)
  • Longitudinal cognitive decline in autosomal-dominant Alzheimer's disease varies with mutations in APP and PSEN1 genes
  • 2019
  • Ingår i: Neurobiology of Aging. - : ELSEVIER SCIENCE INC. - 0197-4580 .- 1558-1497. ; 82, s. 40-47
  • Tidskriftsartikel (refereegranskat)abstract
    • The purpose was to compare longitudinal cognitive changes in APP and PSEN1 gene mutation carriers and noncarriers from four autosomal-dominant Alzheimer's disease (ADAD) families across preclinical and early clinical stages of disease. Carriers (n = 34) with four different mutations (PSEN1(M146V), PSEN1(H163Y), APP(SWE), and APP(ARC)) and noncarriers (n = 41) were followed up longitudinally with repeated cognitive assessments starting many years before the expected clinical onset. The relationship between cognition and years to expected clinical onset, education, age, and type of mutation was analyzed using mixed-effects models. Results showed an education-dependent and time-related cognitive decline with linear and quadratic predictors in mutation carriers. Cognitive decline began close to the expected clinical onset and was relatively rapid afterward in PSEN1 mutation carriers, whereas decline was slower and started earlier than 10 years before expected clinical onset in APP mutation carriers. In noncarriers, the decline was minimal across time in accordance with normal aging. These results suggest that phenotypes for onset and rate of cognitive decline vary with PSEN1 and APP genes, suggesting a behavioral heterogeneity in ADAD. (C) 2019 Elsevier Inc. All rights reserved.
  • Andersson, A, et al. (författare)
  • Platelet [3H]paroxetine binding to 5-HT uptake sites in Alzheimer's disease.
  • 1991
  • Ingår i: Neurobiology of Aging. - 0197-4580 .- 1558-1497. ; 12:5, s. 531-4
  • Tidskriftsartikel (refereegranskat)abstract
    • Platelet serotonin (5-hydroxytryptamine, 5-HT) uptake sites were studied in a control group (n = 30) and an Alzheimer group (n = 40) using [3H]paroxetine as radioligand. The maximum number of binding sites (Bmax) for control (1250 +/- 60 fmol/mg protein) was not different from the Alzheimer group (1280 +/- 40 fmol/mg protein). There were no differences in apparent binding affinity (Kd): 0.046 (0.024-0.062) nM for control and 0.040 (0.027-0.061) nM for Alzheimer. Thus even though several previous studies have demonstrated marked atrophy of 5-HT containing neurites and 5-HT uptake sites in Alzheimer's disease, these findings are not found in the periphery on platelets. The platelet 5-HT uptake site cannot be used as a peripheral marker of Alzheimer's disease.
  • Andersson, Christin, et al. (författare)
  • Increasing CSF phospho-tau levels during cognitive decline and progression to dementia
  • 2008
  • Ingår i: Neurobiology of Aging. - 0197-4580 .- 1558-1497. ; 29:10, s. 1466-1473
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Little is known about longitudinal changes of cerebrospinal fluid (CSF) biomarkers during cognitive decline in neurodegenerative disease progression. Objective To investigate longitudinal changes in CSF biomarkers – total-tau (T-tau), phospho-tau (P-tau) and β-amyloid (Aβ42) – during cognitive decline. Methods Forty memory clinic patients (47.5% females), aged 61.3 ± 7.6 (S.D.) years, non-demented at baseline, underwent lumbar puncture and neuropsychological testing at two occasions. Baseline mean MMSE-score was 28.3 ± 1.8. Patients were divided into three groups based on baseline memory functioning; severely impaired (SIM), moderately impaired (MIM) and no impairment (NIM). Results There was a significant increase in P-tau in the SIM-group during follow-up, while P-tau in MIM and NIM did not change. Eighty-three percent of the SIM-patients converted to dementia (80% AD), while most MIM- and NIM-patients remained non-demented. T-tau- and Aβ42-levels did not change in any of the memory groups during follow-up. Conclusion Increasing P-tau levels during cognitive decline and conversion to dementia suggest that P-tau may be useful as a longitudinal marker of the neurodegenerative process.
  • Andersson, Pernilla, 1992-, et al. (författare)
  • The association between control of interference and white-matter integrity : A cross-sectional and longitudinal investigation
  • 2022
  • Ingår i: Neurobiology of Aging. - : Elsevier. - 0197-4580 .- 1558-1497. ; 114, s. 49-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Proactive interference (PI) occurs when old information interferes with newly acquired information and has been suggested as a major cause of forgetting in working memory. In this study, we investigate cross-sectional (N = 267) and longitudinal (N = 148) associations between PI and white-matter integrity (WMI) using diffusion-weighted imaging in an adult life-span sample (25-80 years; Mage = 60.15; 138 female). Older age was related to higher PI and lower WMI. Cross-sectional analyses showed associations between PI and WMI spanning several white-matter tracts as well as globally, suggesting that the age-related decline in PI may be driven primarily by global changes in WMI. Furthermore, longitudinal changes in PI were shown to be negatively correlated with concurrent changes in WMI in the fornix. Mediation analyses showed that WMI mediated the relationship between age and PI only in older adults, indicating that WMI becomes increasingly connected to cognitive functioning with increasing age. This is the first demonstration of WMI decline contributing to the age-related decline in PI.
  • Ashton, Nicholas J., et al. (författare)
  • No association of salivary total tau concentration with Alzheimer's disease.
  • 2018
  • Ingår i: Neurobiology of aging. - : Elsevier. - 1558-1497 .- 0197-4580. ; 70, s. 125-127
  • Tidskriftsartikel (refereegranskat)abstract
    • There is a need for an accessible biomarker that can complement current cerebrospinal fluid and imaging biomarkers in an accurate and early diagnosis of Alzheimer disease (AD). Saliva is a rich source of potential biomarkers and proteins related to neurodegenerative disorders have been shown to be present in this matrix, including tau. In this study, we quantified salivary total tau (t-tau) concentration in 160 healthy elderly control, 68 mild cognitive impairment, and 53 AD participants using ultrasensitive Single molecule array (Simoa) technology. No median difference in salivary t-tau concentration was found between AD and mild cognitive impairment or healthy elderly control (12.3 ng/L, 9.8 ng/L and 9.6 ng/L, respectively, p = 0.219). In addition, there was no association of salivary t-tau concentration with neurophysiological assessment or structural magnetic resonance imaging. Despite a nominal increase in AD, due to the large overlaps in concentrations between clinical groups, we conclude that salivary t-tau is a suitable biomarker neither for AD nor for cognitive impairment.
  • Avelar-Pereira, Bárbara, et al. (författare)
  • Increased functional homotopy of the prefrontal cortex is associated with corpus callosum degeneration and working memory decline
  • 2020
  • Ingår i: Neurobiology of Aging. - : Elsevier. - 0197-4580 .- 1558-1497. ; 96, s. 68-78
  • Tidskriftsartikel (refereegranskat)abstract
    • Functional homotopy reflects the link between spontaneous activity in a voxel and its counterpart in the opposite hemisphere. Alterations in homotopic functional connectivity (FC) are seen in normal aging, with highest and lowest homotopy being present in sensory-motor and higher-order regions, respectively. Homotopic FC relates to underlying structural connections, but its neurobiological underpinnings remain unclear. The genu of the corpus callosum joins symmetrical parts of the prefrontal cortex (PFC) and is susceptible to age-related degeneration, suggesting that PFC homotopic connectivity is linked to changes in white-matter integrity. We investigated homotopic connectivity changes and whether these were associated with white-matter integrity in 338 individuals. In addition, we examined whether PFC homotopic FC was related to changes in the genu over 10 years and working memory over 5 years. There were increases and decreases in functional homotopy, with the former being prevalent in subcortical and frontal regions. Increased PFC homotopic FC was partially driven by structural degeneration and negatively associated with working memory, suggesting that it reflects detrimental age-related changes.
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