Previous studies indicate that tau protein, a marker of damage to neurons, is present in the serum of healthy patients at a concentration approximately 40 percent that of patients with ischemic stroke We assumed that increased serum activity of gelatinases (matrix metalloproteinase [MMP]-2 and MMP-9) can influence the level of tau protein in serum, probably due to disruption of the blood-brain barrier. We obtained blood sera from 31 patients admitted within the first 24 hours of ischemic stroke on days 1, 5 and 10, following the onset of stroke. Tau protein was detected in the serum of 12 patients (38.7 percent). The highest MMP-9 activity was recorded on day 5 (p < 0.05). Serum gelatinase activity did not differ between tau protein-positive or -negative individuals. However, a high degree of correlation between mean MMP-9 activity and the maximum tau protein level was observed for patients with detectable tau protein (r = 0.71, p = 0.009). Our study suggests that MMP-9 can increase the tau protein level in the sera of patients during acute ischemic stroke.
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http://dx.doi.org/10.1016/j.jocn.2010.01.005 | DOI Listing |
Neurol Int
December 2024
Department of Obstetrics, Gynecology and Reproductive Sciences, School of Medicine, University of Miami Miller, Miami, FL 33136, USA.
Neurosyphilis-induced dementia represents a severe manifestation of tertiary syphilis, characterized by cognitive and neuropsychiatric impairments. This condition arises from the progression of syphilis to the central nervous system, where the spirochete causes damage through invasion, chronic inflammation, and neurodegeneration. The pathophysiology involves chronic inflammatory responses, direct bacterial damage, and proteinopathies.
View Article and Find Full Text PDFFront Cell Neurosci
December 2024
Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Introduction: Abnormal intracellular accumulation of Tau aggregates is a hallmark of Alzheimer's disease (AD) and other Tauopathies, such as Frontotemporal dementia (FTD). Tau deposits primarily affect neurons, but evidence indicates that glial cells may also be affected and contribute distinctively to disease progression. Cells can respond to toxic insults by orchestrating global changes in posttranslational modifications of their proteome.
View Article and Find Full Text PDFJ Clin Periodontol
December 2024
Department of Periodontics, Liaoning Provincial Key Laboratory of Oral Diseases, School and Hospital of Stomatology, China Medical University, Shenyang, China.
Aim: Porphyromonas gingivalis, a consensus periodontal pathogen, is thought to be involved in Alzheimer's disease (AD) progression, and P. gingivalis-derived outer membrane vesicles (PgOMVs) are a key toxic factor in inducing AD pathology. This study aimed to clarify the regulatory mechanism underlying the PgOMV-induced AD-like phenotype.
View Article and Find Full Text PDFAlzheimers Res Ther
December 2024
Laboratory of Neurodegenerative Diseases, Center for Biomedicine, Universidad Mayor, Temuco, Chile.
In recent years, a growing body of research has unveiled the involvement of the necroptosis pathway in the pathogenesis of Alzheimer's disease (AD). This evidence has shed light on the mechanisms underlying neuronal death in AD, positioning necroptosis at the forefront as a potential target for therapeutic intervention. This review provides an update on the current knowledge on this emerging, yet rapidly advancing topic, encompassing all published studies that present supporting proof of the role of the necroptosis pathway in the neurodegenerative processes of AD.
View Article and Find Full Text PDFBrain Res
December 2024
Federal University of São Paulo, Paulista School of Medicine, Department of Physiology, Laboratory of Neurophysiology, São Paulo, Brazil.
Alzheimer's disease is a progressive neurodegenerative disease affecting memory, language, and thinking with no curative treatment. Symptoms appear gradually, and pathological brain changes may occur twenty years before the physical and psychological signs, pointing to the urgent development of preventive interventions. Physical activity has been investigated as a preventive tool to defeat the main biological features of AD: pathological amyloid protein plaques, tau tangles, myelin degeneration, and iron deposits in the brain.
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