Simplified procedures were developed to produce and isolate the plasmin-derived B beta 1-42 fragment from human fibrinogen. Peptides generated from fibrinogen by plasmin were separated by reverse phase HPLC chromatography. Two distinct peaks were identified as having amino acid compositions identical to B beta 1-42. The average final yield of HPLC-purified B beta 1-42 was 1.2 mg per 100 mg of fibrinogen. Recovery of the peptide (40-45% when compared to the theoretical yield) was significantly higher than yields obtained by open column techniques demonstrating the advantages of this simple one-step HPLC procedure.
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http://dx.doi.org/10.1016/0049-3848(86)90226-4 | DOI Listing |
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.
Antioxidants (Basel)
January 2025
Department of Pharmacy, University of Salerno, Via Giovanni Paolo II, 132, 84084 Fisciano, Italy.
Investigating amyloid-β (Aβ) peptides in solution is essential during the initial stages of developing lead compounds that can influence Aβ fibrillation while the peptide is still in a soluble state. The tendency of the Aβ(1-42) peptide to misfold in solution, correlated to the aetiology of Alzheimer's disease (AD), is one of the main hindrances to characterising its aggregation kinetics in a cell-mimetic environment. Moreover, the Aβ(1-42) aggregation triggers the unfolded protein response (UPR) in the endoplasmic reticulum (ER), leading to cellular dysfunction and multiple cell death modalities, exacerbated by reactive oxygen species (ROS), which damage cellular components and trigger inflammation.
View Article and Find Full Text PDFJ Neurol
January 2025
Alzheimer's Disease and Other Cognitive Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, Fundació de Recerca Clínic - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Villaroel 170, 08036, Barcelona, Spain.
Plasma tau phosphorylated at threonine 181 (p-tau181) and 217 (p-tau217) have demonstrated high accuracy for Alzheimer's disease (AD) diagnosis, defined by CSF/PET amyloid beta (Aβ) positivity, but most studies have been performed in research cohorts, limiting their generalizability. We studied plasma p-tau217 and p-tau181 for CSF Aβ status discrimination in a cohort of consecutive patients attending an academic memory clinic in Spain (July 2019-June 2024). All patients had CSF AD biomarkers performed as part of their routine clinical assessment.
View Article and Find Full Text PDFESMO Open
January 2025
Dana-Farber Cancer Institute, Boston, USA. Electronic address:
Background: Lu-prostate-specific membrane antigen (PSMA)-617 (LuPSMA) is a radionuclide therapy approved for patients with PSMA-avid metastatic castrate-resistant prostate cancer (mCRPC). We evaluated whether alterations in the DNA damage repair (DDR) pathway were associated with outcomes to LuPSMA.
Patients And Methods: We identified an institutional cohort of men (n = 134) treated with ≥2 cycles of LuPSMA who had panel-based germline and/or tumor genomic sequencing.
Int J Biol Macromol
January 2025
College of Pharmacy, Chung-Ang University, 84 Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea. Electronic address:
Alzheimer's disease (AD) is characterized as a neurodegenerative disorder that is caused by plaque formation by accumulating β-amyloid (Aβ), leading to neurocognitive function and impaired mental development. Thus, targeting Aβ represents a promising target for the development of therapeutics in AD management. Several functionalized sulfonic acid molecules have been reported, including tramiprosate prodrug, which is currently in clinical trial III and exhibits a good response in mild to moderate AD patients.
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