According to the modified Boston criteria, cerebral amyloid angiopathy (CAA) can present with lobar hematoma (LH) or superficial siderosis (SS). Recently, decreased CSF β-amyloid peptide 40 and 42 (Aβ40; Aβ42) and increased total and phosphorylated tau (t-tau; p-tau) concentrations have been described in CAA presenting with LH. Our aim was to analyze CSF biomarkers as a diagnostic tool for CAA according to the modified Boston criteria. We prospectively included patients with possible or probable CAA according to the modified Boston criteria. CSF was analyzed for t-tau, p-tau, Aβ42, and Aβ40. Data were compared with AD patients (n = 42) and controls (n = 14). Thirteen CAA patients were included, nine presenting with LH and four with SS. T-tau and p-tau levels in CAA were higher than controls, but lower than in AD. Differences in t-tau and p-tau levels between CAA versus controls and AD were all significant apart of the CAA p-tau levels comparison with controls. Aβ42 levels in CAA were significantly lower than in controls, and slightly higher than in AD, though non-significantly. Aβ40 levels in CAA were non-significantly lower than in controls, and significantly lower than in AD. Combining the findings of our study and the earlier report, we confirm that patients with suspected CAA have significantly different values for t-tau, Aβ42, Aβ42/t-tau, and Aβ40. Especially Aβ40 levels seem to be of clinical interest to differentiate CAA from AD. CSF biomarkers have to be analyzed in a larger number of CAA patients, and compared to patients with other disorders causing LH or SS.
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J Comp Eff Res
January 2025
Boston Scientific Corporation; 100 Boston Scientific Way, Marlborough, MA, USA.
This study assessed the economic impact of reducing one postoperative visit following inflatable penile prosthesis (IPP) implantation. Scenario analyses were used to model the effects of eliminating one 30-min IPP postoperative visit from the expected 2.5 visits accounted for by the American Medical Association resource-based relative value scale data.
View Article and Find Full Text PDFFront Psychol
December 2024
Department of Neurology, Harvard Medical School, Boston, MA, United States.
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April 2025
Brigham MS Center (MKH), Harvard Medical School, Boston, MA; Georgia State University (MCM), Atlanta; Brigham and Women's Hospital (TDM, JP-P, CS, JZ), Boston, MA; Massachusetts General Hospital (ECK), Harvard Medical School, Boston, MA; University of Vermont (AJS), Burlington; Elliot Lewis MS Center (EL, JK), Wellesley, MA; University of Massachusetts (CI, IB), Worcester, MA; Novartis Pharmaceuticals (JMS), Jersey City, NJ; Concord Hospital (AC), NH; and University of British Columbia (ADS), Vancouver, BC, Canada.
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View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Department of Pharmacy The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation.
View Article and Find Full Text PDFNat Med
January 2025
Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Prion disease is a fatal neurodegenerative disease caused by the misfolding of prion protein (PrP) encoded by the PRNP gene. While there is currently no cure for the disease, depleting PrP in the brain is an established strategy to prevent or stall templated misfolding of PrP. Here we developed in vivo cytosine and adenine base strategies delivered by adeno-associated viruses to permanently modify the PRNP locus to achieve PrP knockdown in the mouse brain.
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