Beta 2-microglobulin (beta 2M) amyloidosis is common in patients on long-term hemodialysis, but the clinical conditions associated with disease activity are poorly understood. This study was designed to determine if the serum amyloid P (AP) component concentration is predictive of beta 2M amyloid disease activity. Serum AP component concentrations were determined by rocket immunoelectrophoresis and beta 2M concentrations by a commercially available kit. Radiographic evidence of beta 2M amyloidosis was determined from bone films of the hips, shoulders, and hands. Serum AP component concentrations were not different in dialysis and control patients. However, AP component concentrations in long-term (greater than or equal to 5 years) dialysis patients were significantly lower than in short-term (less than 5 years) dialysis patients (43.0 +/- 16.9 micrograms/mL [n = 28] v 56.0 +/- 18.3 micrograms/mL [n = 31], P less than 0.05). The patients on hemodialysis for 5 or more years who had radiographic evidence of severe beta 2 M amyloidosis were significantly older (57.9 +/- 9.5 v 38.3 +/- 11.3 years, P less than 0.001) and their serum AP concentrations were significantly lower (34.3 +/- 15.0 v 50.1 +/- 15.6 micrograms/mL, P less than 0.05) than long-term dialysis patients without radiographic evidence of disease. Stepwise regression analysis showed that the patient's age and serum AP component concentration were predictors of radiographic evidence of beta 2 M amyloidosis. Thus, serum AP component concentrations are decreased in long-term dialysis patients, suggesting accelerated deposition into amyloid deposits.(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1016/s0272-6386(12)80949-8 | DOI Listing |
Curr Opin Neurol
February 2025
Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands.
Purpose Of Review: Cerebral amyloid angiopathy (CAA) is a common brain disorder among the elderly and individuals with Alzheimer's disease, where accumulation of amyloid-ß can lead to intracerebral hemorrhage and dementia. This review discusses recent developments in understanding the pathophysiology and phenotypes of CAA.
Recent Findings: CAA has a long preclinical phase starting decades before symptoms emerge.
Open Respir Arch
November 2024
Translational Research In Airway Diseases Group (TRIAD), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Respiratory diseases and cardiovascular diseases (CVDs) have high prevalence and share common risk factors. In some respiratory diseases such as sleep apnoea and COPD, the evidence of their negative impact on the prognosis of CVDs seems clear. However, in other diseases it is less evident whether there is any direct relationship.
View Article and Find Full Text PDFNefrologia (Engl Ed)
January 2025
Nephrology Service, University Hospital Reina Sofia, Cordoba-Spain; Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Cordoba, Spain University of Cordoba, Cordoba, Spain; Redes de Investigación Cooperativa Orientadas a Resultados en Salud, RICORS2040, Institute of Health Carlos III, Madrid, Spain; European Uremic Toxins Group (EUTOx). Electronic address:
Neurobiol Aging
December 2024
Vanderbilt Memory and Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA; Pharmacology Department, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, USA; Epidemiology Doctoral Program, School of Medicine, Vanderbilt University, Nashville, TN, USA; Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address:
We have identified FLT1 as a protein that changes during Alzheimer's disease (AD) whereby higher brain protein levels are associated with more amyloid, more tau, and faster longitudinal cognitive decline. Given FLT1's role in angiogenesis and immune activation, we hypothesized that FLT1 is upregulated in response to amyloid pathology, driving a vascular-immune cascade resulting in neurodegeneration and cognitive decline. We sought to determine (1) if in vivo FLT1 levels (CSF and plasma) associate with biomarkers of AD neuropathology or differ between diagnostic staging in an aged cohort enriched for early disease, and (2) whether FLT1 expression interacts with amyloid on downstream outcomes, such as phosphorylated tau levels and cognitive performance.
View Article and Find Full Text PDFNeurology
January 2025
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX; and.
Objectives: Cerebral microbleeds (cMBs) are common imaging findings in conditions related to cerebral amyloid angiopathy (CAA). Blood-brain barrier (BBB) leakage is considered pivotal in their pathogenesis. This study investigates the potential role of cerebral microenhancement (cME) as an imaging biomarker on 3D T1 black-blood MRI (BB-MRI) for BBB rupture, predicting the formation of cMBs in inflammatory CAA variants.
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