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Evaluating amyloid-beta aggregation and toxicity in transgenic Caenorhabditis elegans models of Alzheimer's disease.
Methods Cell Biol
January 2025
Federal University of Santa Maria, Center for Natural and Exact Sciences, Department of Biochemistry and Molecular Biology, Graduate Program in Biological Sciences: Toxicological Biochemistry, Camobi, Santa Maria, RS, Brazil.
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms.
View Article and Find Full Text PDFThe current models unravel the molecular mechanisms underlying the intricate pathophysiology of Alzheimer's disease using zebrafish.
Methods Cell Biol
January 2025
Department of Pharmacology, SPP School of Pharmacy & Technology Management, Mumbai, India. Electronic address:
The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities.
View Article and Find Full Text PDFCore blood biomarkers of Alzheimer's disease: A single-center real-world performance study.
J Prev Alzheimers Dis
February 2025
Neurology, Fondazione IRCCS "San Gerardo dei Tintori", Monza, Italy; Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Monza, Italy; Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy. Electronic address:
Background: The new criteria for Alzheimer's disease pave the way for the introduction of core blood biomarkers of Alzheimer's disease (BBAD) into clinical practice. However, this depends on the demonstration of sufficient accuracy and robustness of BBADs in the intended population.
Objectives: To assess the diagnostic performance of core BBADs in our memory clinic, comparing them with cerebrospinal fluid (CSF) analysis.
Microstructural white matter injury contributes to cognitive decline: Besides amyloid and tau.
J Prev Alzheimers Dis
February 2025
Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, PR China. Electronic address:
Background: Cognitive decline and the progression to Alzheimer's disease (AD) are traditionally associated with amyloid-beta (Aβ) and tau pathologies. This study aims to evaluate the relationships between microstructural white matter injury, cognitive decline and AD core biomarkers.
Methods: We conducted a longitudinal study of 566 participants using peak width of skeletonized mean diffusivity (PSMD) to quantify microstructural white matter injury.
Distinct CSF α-synuclein aggregation profiles associated with Alzheimer's disease phenotypes and MCI-to-AD conversion.
J Prev Alzheimers Dis
February 2025
The ADNI is detailed in Supplemental Acknowledgments.
Background: α-Synuclein (α-Syn) pathology is present in 30-50 % of Alzheimer's disease (AD) patients, and its interactions with tau proteins may further exacerbate pathological changes in AD. However, the specific role of different aggregation forms of α-Syn in the progression of AD remains unclear.
Objectives: To explore the relationship between various aggregation types of CSF α-Syn and Alzheimer's disease progression.
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