The association between verbal fluency deficit in Alzheimer's disease (AD) and deterioration of specific white matter (WM) tracts is currently not well understood. Using diffusion tensor imaging, we investigated a possible association between the left uncinate fasciculus, which has been implicated in word retrieval, and verbal fluency deficit in AD. A comparison of five properties of WM (fractional anisotropy, mode of anisotropy, mean diffusivity, radial diffusivity, and axial diffusivity) in 28 mild AD patients and 26 age-, gender- and education-matched healthy controls revealed significant group differences in a range of WM tracts. Looking specifically at diffusion parameters' values for the left uncinate fasciculus and verbal fluency scores in the AD group, we observed a positive trend between the letter fluency scores and mode of anisotropy values ( = 0.36, = 0.55). Thus, our data suggest more global WM damage in mild AD, which also includes damage to the left uncinate fasciculus. However, damage to this particular tract is not robustly associated with verbal fluency decline at this stage of disease.
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http://dx.doi.org/10.1515/tnsci-2016-0014 | DOI Listing |
Alzheimers Dement
December 2024
The Fourth People's Hospital of Chengdu, Chengdu, Sichuan, China.
Background: Apolipoproteins and cortical morphology are closely associated with memory complaints, and both may contribute to the development of Alzheimer's disease.
Method: A total of 97 patients from the University of Electronic Science and Technology (UESTC) (n=42) and the Fourth People's Hospital of Chengdu (FPHC) (n=55) were grouped based on recruitment location, and underwent neuropsychological tests. ApoB, ApoA1, ApoB/ApoA1, plasma Alzheimer's biomarker, apolipoprotein E (ApoE) genotyping, 3T magnetic resonance imaging.
Alzheimers Dement
December 2024
German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany.
Background: Speech abnormalities are increasingly recognized as a manifestation of cognitive deficits in Alzheimer's disease (AD) and its preclinical and prodromal stages. Here, we investigated whether MRI measures of brain atrophy, specifically in the basal forebrain and cortical language areas, can predict cognitive decline and speech difficulties in older adults within the AD spectrum.
Method: The ongoing Prospect-AD study aims to develop an algorithm to automatically identify speech biomarkers in individuals with early signs of AD.
Alzheimers Dement
December 2024
Cognitive Neuroscience Center, University of San Andrés, Victoria, Buenos Aires, Argentina.
Background: Beyond dementia syndromes, cognitive symptoms are highly prevalent in Parkinson's disease (PD), often manifesting as mild cognitive impairment (MCI). Yet, their detection and characterization remain suboptimal because standard approaches rely on subjective impressions derived from lengthy, univariate tests. Here we introduce a novel approach to detect cognitive symptom severity and identify MCI in PD using fully automated word property analyses on brief verbal fluency tasks.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
National Institute of Mental Health, Neurology and Neurosurgery, Budapest, Hungary.
Background: Growing evidence suggests that the imbalance between excitability and inhibitory neural activity is a key aspect of cognitive decline. Subclinical epileptiform activity (SEA) has been indicated as a marker of increased cortical excitability. While SEA is considered as a benign EEG sign in the elderly population, recent studies demonstrated its role in the progression of Alzheimer's disease.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory of Clinical Investigation, National Institute on Aging, Intramural Research Program, Baltimore, MD, USA.
Background: The choroid plexus (CP), a vital component in the brain's ventricles, is crucial for cerebrospinal fluid (CSF) production and maintenance of the brain's physiological environment. It plays a key role in regulating neuroinflammatory responses, clearing harmful substances, producing neurotrophic factors and signaling molecules, and forming blood-CSF barrier. Consequently, changes to the CP's structural integrity could disrupt brain homeostasis and lead to cognitive impairment.
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