36 research outputs found

    Brain Volume Differences and Proactive Interference: A VBM Investigation of Healthy Cognitive Aging.

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    Research on aging and memory has consistently demonstrated decreased memory performance in older adults, specifically on tasks measuring verbal and spatial memory. Memory decline in aging is partially related to interference from competing information. In older adults, the learning of new information is more adversely affected by already-formed memories (i.e. proactive interference) than in younger adults. However, interference of new information on already- formed memories (retroactive interference) is less affected by age. The present investigation examined the association between proactive and retroactive interference, and brain volume in young and older adults. Proactive and retroactive interference were assessed with a Modified modified free recall (MMFR) test. Participants (n=39) first studied AB and DE word pairs three times before undergoing a cued recall test. Following AB-DE testing, participants had only one study-test cycle of AC and FG word pairs. Finally, participants completed the MMFR test to evaluate their memory for all previously studied and tested words. Results revealed that older adults experienced significantly more proactive interference than younger adults (performance on MMFR-AC minus MMFR-FG), but both age groups performed similarly on the retroactive interference measures. It was hypothesized that brain volume, and specifically Hippocampal and prefrontal volume, would be significantly correlated to memory performance; however no significant correlations were found with any specific brain regions

    Differences in hippocampal subfield volume are seen in phenotypic variants of early onset Alzheimer's disease.

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    The most common presentation of early onset Alzheimer's disease (EOAD - defined as symptom onset <65 years) is with progressive episodic memory impairment - amnestic or typical Alzheimer's disease (tAD). However, EOAD is notable for its phenotypic heterogeneity, with posterior cortical atrophy (PCA) - characterised by prominent higher-order visual processing deficits and relative sparing of episodic memory - the second most common canonical phenotype. The hippocampus, which comprises a number of interconnected anatomically and functionally distinct subfields, is centrally involved in Alzheimer's disease and is a crucial mediator of episodic memory. The extent to which volumes of individual hippocampal subfields differ between different phenotypes in EOAD is unclear. The aim of this analysis was to investigate the hypothesis that patients with a PCA phenotype will exhibit differences in specific hippocampal subfield volumes compared to tAD. We studied 63 participants with volumetric T1-weighted MRI performed on the same 3T scanner: 39 EOAD patients [27 with tAD and 12 with PCA] and 24 age-matched controls. Volumetric estimates of the following hippocampal subfields for each participant were obtained using Freesurfer version 6.0: CA1, CA2/3, CA4, presubiculum, subiculum, hippocampal tail, parasubiculum, the molecular and granule cell layers of the dentate gryus (GCMLDG), the molecular layer, and the hippocampal amygdala transition area (HATA). Linear regression analyses comparing mean hippocampal subfield volumes between groups, adjusting for age, sex and head size, were performed. Using a Bonferonni-corrected p-value of p < 0.0025, compared to controls, tAD was associated with atrophy in all hippocampal regions, except the parasubiculum. In PCA patients compared to controls, the strongest evidence for volume loss was in the left presubiclum, right subiculum, right GCMLDG, right molecular layer and the right HATA. Compared to PCA, patients with tAD had strong evidence for smaller volumes in left CA1 and left hippocampal tail. In conclusion, these data provide evidence that hippocampal subfield volumes differ in different phenotypes of EOAD

    Medial temporal lobe atrophy on MRI: vascular risk factors and predictive value for dementia

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    Barkhof, F. [Promotor]Scheltens, P. [Promotor]Launer, L.J. [Copromotor
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