The aim of this work is to present whether SPECT Tc-HMPAO can be a method of examination to possibly differentiate the syndromes. 21 patients with PSP syndrome and 14 patients with corticobasal syndrome (CBS) were examined using SPECT Tc-HMPAO. Perfusion single photon emission computed tomography (SPECT) as a method of examination of progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) has not been extensively analyzed in contemporary literature. Recent criteria of PSP and CBS do not describe this method of examination as primary or additional. Extended analysis was done in the context of regions of interest affected by significant average hypoperfusion (>2 standard deviations). Differences between the syndromes were subsequently evaluated using the U-Mann-Whitney test. Lack of significant differences (p < 0.05) were observed in 92 out of 94 regions of interest. However, certain asymmetries were observed in a minority of regions in both of the syndromes. Additionally, the authors of the study verified possible differences of asymmetry of perfusion of both of the syndromes. The overlapping of clinical manifestations and locations of hypoperfusion leads to a question of whether the syndromes should be interpreted as separate entities or variants of the same disease.
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http://dx.doi.org/10.1016/j.jocn.2020.05.005 | DOI Listing |
Alzheimers Dement
December 2024
Alzheimer Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, Amsterdam, Netherlands.
Background: There is a strong link between tau and progression of Alzheimer's disease (AD), necessitating an understanding of tau spreading mechanisms. Prior research, predominantly in typical AD, suggested that tau propagates from epicenters (regions with earliest tau) to functionally connected regions. However, given the constrained spatial heterogeneity of tau in typical AD, validating this connectivity-based tau spreading model in AD variants with distinct tau deposition patterns is crucial.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Memory and Aging Center, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Background: Diagnosing sporadic early-onset AD (EOAD, age-at-onset<65) is challenging: in the multi-center Longitudinal Early-onset Alzheimer's Disease Study, ∼25% of patients with clinically diagnosed EOAD are amyloid-PET-negative. Here we used FDG-PET to characterize the heterogeneity of hypometabolic profiles in these patients and better identify underlying etiologies.
Method: Seventy-four amyloid-PET-negative patients with clinical diagnosis of sporadic EOAD (MCI or mild dementia stage) underwent FDG-PET.
Alzheimers Dement
December 2024
Department of Neurology, University of Pennsylvania, Philadelphia, PA, USA.
Background: Amnestic mild cognitive impairment and Alzheimer's disease (aAD) exhibit degeneration of white matter (WM) tracts preceding overt cognitive decline. However, WM changes in non-amnestic AD (naAD) are understudied. We hypothesized patterns of WM degeneration would differ between aAD and naAD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Università degli studi di Genova, Genova, Liguria, Italy.
Background: Alzheimer's disease (AD) is the most common form of dementia, predominantly manifesting as amnestic impairment. However, atypical presentations such as logopenic variant of primary progressive aphasia (lvPPA), posterior cortical atrophy (PCA), corticobasal syndrome (CBS) and frontal AD pose diagnostic challenges. This study presents preliminary data from a retrospective analysis investigating brain functional differences between typical and atypical AD forms.
View Article and Find Full Text PDFBackground: Progressive supranuclear palsy (PSP) can present with different clinical variants which show distinct, but partially overlapping, patterns of neurodegeneration and tau deposition in a PSP network of regions, including cerebellar dentate, superior cerebellar peduncle, midbrain, thalamus, basal ganglia, and frontal lobe. We sought to determine whether disruptions in functional connectivity within this PSP network measured using resting-state functional MRI (rs-fMRI) differed between PSP-Richardson's syndrome and the cortical and subcortical variants of PSP.
Method: Structural MRI and rs-fMRI scans were collected for 40 PSP-RS, 24 PSP-cortical (12 speech and language; 10 corticobasal syndrome; 2 frontal) and 36 PSP-subcortical (18 parkinsonism; 11 progressive gait freezing; 6 postural instability; 1 oculomotor) participants who met the Movement Disorder Society PSP clinical criteria (Table 1).
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