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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Memory & Aging Center, Department of Neurology, University of California in San Francisco, San Francisco, CA, USA.
Background: Lewy body disease (LBD) often co-occurs with Alzheimer's (AD), resulting in more significant cognitive decline than AD or LBD alone. LBD's hallmarks, asyn-positive Lewy bodies and neurites, propagate from the enteric system or olfactory bulb to the amygdala, which acts as a gatekeeper for spread to other structures. Initially, LBD appears in the central or cortical nuclei, reflecting brainstem or olfactory origins.
View Article and Find Full Text PDFTerminology controversies.
Alzheimers Dement
December 2024
Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
N-terminus α-synuclein detection reveals new and more diverse aggregate morphologies in multiple system atrophy and Parkinson's disease.
Transl Neurodegener
December 2024
Department of Anatomy and Medical Imaging, University of Auckland, 85 Park Road, Grafton, , Auckland, 1142, New Zealand.
Background: Parkinson's disease (PD) and multiple system atrophy (MSA) are classified as α-synucleinopathies and are primarily differentiated by their clinical phenotypes. Delineating these diseases based on their specific α-synuclein (α-Syn) proteoform pathologies is crucial for accurate antemortem biomarker diagnosis. Newly identified α-Syn pathologies in PD raise questions about whether MSA exhibits a similar diversity.
View Article and Find Full Text PDFAccumulation of alpha-synuclein pathology in the liver exhibits post-translational modifications associated with Parkinson's disease.
iScience
December 2024
Department of Biomedical and Clinical Sciences, Department of Clinical Pathology, Linköping University, Linköping, Sweden.
Accumulating evidence demonstrates that alpha-synuclein (α-syn) pathology associated with Parkinson's disease (PD) is not limited to the brain, as it also appears in a select number of peripheral tissues including the liver. In this study, we identified a number of PD-associated α-syn post-translational modifications in the livers of (Thy-1)-h[A30P] mice, a mouse model of familial PD expressing human α-syn harboring the A30P mutation driven by a neuron-specific promoter. , we also demonstrate that human hepatocytes induce post-translational modifications following α-syn fibrillar (PFF) treatment.
View Article and Find Full Text PDFData-driven CSF biomarker profiling: imaging and clinical outcomes in a cohort at risk of Alzheimer's disease.
Alzheimers Res Ther
December 2024
University of Pompeu Fabra (UPF), Barcelona, Spain.
Background: Cerebrospinal fluid (CSF) biomarkers of synaptic dysfunction, neuroinflammation, and glial response, complementing Alzheimer's disease (AD) core biomarkers, have improved the pathophysiological characterization of the disease. Here, we tested the hypothesis that the co-expression of multiple CSF biomarkers will help the identification of AD-like phenotypes when biomarker positivity thresholds are not met yet.
Methods: Two hundred and seventy cognitively unimpaired adults with family history (FH) of sporadic AD (mean age = 60.
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