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Decoding Alzheimer's Disease With Depression: Molecular Insights and Therapeutic Target.
J Cell Mol Med
March 2025
Department of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, P. R. China.
The purpose of this study was to recognise predictive biomarkers and explore the promising therapeutic targets of AD with depression. We confirmed a positive correlation between AD and depression through MR Analysis. Through WGCNA analysis, we identified 1569 genes containing two modules, which were most related to AD.
View Article and Find Full Text PDFPhosphorylation-Induced Self-Coacervation versus RNA-Assisted Complex Coacervation of Tau Proteins.
J Am Chem Soc
March 2025
Institute of Biological Chemistry, Academia Sinica, No. 128, Sec. 2, Academia Road, Nankang, Taipei 115, Taiwan.
In this study, the role of phosphorylation in the liquid-liquid phase separation (LLPS) of tau, the underlying driving forces, and the potential implications of this separation on protein conformation and subsequent protein aggregation were investigated. We compared in vivo-produced phosphorylated tau (p-tau) and nonphosphorylated tau under different coacervation conditions without adding crowding agents. Our findings revealed that spontaneous phase separation occurs exclusively in p-tau, triggered by a temperature shift from 4 °C to room temperature, and is driven by electrostatic and hydrophobic interactions.
View Article and Find Full Text PDFMulti-omics analysis of druggable genes to facilitate Alzheimer's disease therapy: A multi-cohort machine learning study.
J Prev Alzheimers Dis
March 2025
Department of Pathophysiology School of Basic Medicine Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Background: The swift rise in the prevalence of Alzheimer's disease (AD) alongside its significant societal and economic impact has created a pressing demand for effective interventions and treatments. However, there are no available treatments that can modify the progression of the disease.
Methods: Eight AD brain tissues datasets and three blood datasets were obtained.
Hemispheric asymmetry in neurodegenerative diseases.
Handb Clin Neurol
March 2025
University School for Advanced Studies (IUSS-Pavia), Pavia, Italy; Dementia Research Center, IRCCS Mondino Foundation, Pavia, Italy. Electronic address:
Hemispheric asymmetry in pathologic involvement is frequently observed in neurodegenerative disorders (NDD) and is responsible for differences in cognitive and motor clinical manifestations in individual patients. While asymmetry is modest in typical Alzheimer disease (AD), atypical AD presentations with prominent language impairment [logopenic/phonologic variant of primary progressive aphasia (L/Phv-PPA)] are associated with prevalent involvement of the language-dominant hemisphere. Similarly, in the frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) spectrum, the semantic (Sv) and nonfluent/agrammatic (Nf/Av) variants of PPA are due to asymmetric pathology involving the language-dominant hemisphere.
View Article and Find Full Text PDFExplore peptides extracted from gliadin hydrolysates suppressing BACE1 activity and restraining Aβ protein deposition.
Int J Biol Macromol
March 2025
Institute of Translational Medicine and New Drug Development, China Medical University, Taichung 404333, Taiwan; Department of Biomedical Sciences and Engineering, Tzu Chi University, Hualien 970374, Taiwan. Electronic address:
Alzheimer's Disease (AD) constitutes approximately 70 % of dementia cases and is the most prevalent form of dementia. Current therapeutic options, including acetylcholinesterase inhibitors and N-methyl d-aspartate (NMDA) receptor antagonists, provide symptomatic relief but do not cure the disease and often come with side effects. The primary pathological features of AD are amyloid plaques and neurofibrillary tangles, with amyloid plaques formed by the abnormal accumulation of Amyloid-β (Aβ).
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