Objective: To investigate the independent associations between medial temporal lobe atrophy and white matter hyperintensities (WMH) and cognitive functions in the elderly.
Methods: Cognitive functions of 41 Alzheimer's disease patients, 20 patients with mild cognitive impairment and 28 elderly subjects without memory complaints were assessed using a neuropsychological test battery. Quantitative MRI measures of medial temporal lobe volume and WMH were obtained. Multiple regression analyses were performed to assess the independent contribution of MRI measures to impairment in several cognitive functions.
Results: Scores on the Wechsler Memory Scale and Trails B depended selectively on medial temporal lobe volume, whereas WMH selectively contributed to performance on Trails A. Medial temporal lobe volume and WMH both contributed to scores on the Cambridge Cognitive Examination and the Boston naming task.
Conclusions: MRI measures suggestive of Alzheimer-type pathology and microvascular pathology independently contribute to cognitive decline at old age. Memory impairment as measured using the Wechsler Memory Scale and performance on Trails B primarily depended on medial temporal lobe atrophy. Psychomotor slowness, as measured using Trails A, mainly depended on WMH. These results suggest that vascular pathology and Alzheimer-type pathology each have specific cognitive correlates.
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http://dx.doi.org/10.1159/000086072 | DOI Listing |
Alzheimers Dement
December 2024
Rutgers University-Newark, Newark, NJ, USA.
Background: Alzheimer's disease (AD) is sometimes characterized as "type 3 diabetes" because hyperglycemia impairs cognitive function, particularly in the medial temporal lobe (MTL) and prefrontal regions. Further, both AD and type 2 diabetes (T2D) disproportionately impact African Americans. Although people with T2D are generally suggested to have lower episodic memory and executive function, limited data exist in older African Americans.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Allen Institute for Brain Science, Seattle, WA, USA.
Background: Alzheimer's Disease is marked by the gradual aggregation of pathological proteins, Tau and beta-amyloid, throughout various areas of the brain. The progression of these pathologies follows a consistent pattern, impacting various cellular populations as it advances through each brain region. Previously, we used Bayesian algorithms to create a continuous progression score to mathematically capture the collective aggregation of multiple pathological variables within a specific brain region.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Cerebral small vessel disease (CSVD), which includes cerebral amyloid angiopathy (CAA) and arteriolosclerosis, often co-occurs with Alzheimer's disease (AD) pathology. The medial temporal lobe (MTL) is susceptible to hosting multiple AD pathologies, such as neurofibrillary tangles (NFTs), amyloid-β plaques, phospho-Tar-DNA-Binding-Protein-43 (pTDP-43), as well as CSVD. Whether a causal relationship between these pathologies exists remains largely unknown, but one potential linking mechanism is the dysfunction of perivascular clearance.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, San Francisco, Weill Institute for Neurosciences, San Francisco, CA, USA.
Background: Alzheimer's disease (AD) and other dementia risk may be influenced by the immune function and associated with several white blood cell type counts. In cognitively normal Black, Hispanic, and non-Hispanic white older adults we related three white blood cell types previously associated with AD risk to tau positron emission tomography (PET) values in the medial temporal lobe (MTL), where tau accumulates early. We assessed whether amyloid positivity moderated this relationship.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: The Cognitive Function Index (CFI) is a validated test used to assess changes in self-perceived cognitive and functional status as reported by an individual and their study partner. Previous studies have demonstrated an inverse correlation between higher amyloid-beta (Aβ) burden and CFI, with certain CFI items exhibiting stronger associations than others. However, there is limited understanding of the association between declines in cognition and function, as assessed by CFI, and Tau levels measured by PET.
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