neurodegenerative diseases/albumina

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Differential effects of albumin on microglia and macrophages; implications for neurodegeneration following blood-brain barrier damage.

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Microglial activation by blood-borne factors following blood-brain barrier damage may play a significant role in subsequent neuropathogenesis of several neurodegenerative diseases. Exposure of primary cultured rat brain microglia to pure, fatty acid- and lipid-deficient rat serum albumin or fraction

Blood-derived serum albumin contributes to neurodegeneration via astroglial stress fiber formation.

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Enhanced influx of blood-derived serum albumin into the brain is seen after blood-brain barrier disrupture and may induce neurodegeneration. The aim of the present study was to explore the effects of high levels of bovine serum albumin (BSA) on the survival of cholinergic neurons in organotypic

Cationic albumin-conjugated chelating agent as a novel brain drug delivery system in neurodegeneration.

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The critical role of metal ions and in particular iron in oxidative stress and protein aggregation offers chelation therapy as a sensible pharmaceutical strategy in oxidative stress-induced neuronal damages. In this research, we conjugated an iron-chelating agent, deferasirox, to cationized human

Microglial AGE-albumin is critical in promoting alcohol-induced neurodegeneration in rats and humans.

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Alcohol is a neurotoxic agent, since long-term heavy ingestion of alcohol can cause various neural diseases including fetal alcohol syndrome, cerebellar degeneracy and alcoholic dementia. However, the molecular mechanisms of alcohol-induced neurotoxicity are still poorly understood despite numerous

Deciphering structural intermediates and genotoxic fibrillar aggregates of albumins: a molecular mechanism underlying for degenerative diseases.

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The misfolding and aggregation of proteins is involved in some of the most prevalent neurodegenerative disorders. The importance of human serum albumin (HSA) stems from the fact that it is involved in bio-regulatory and transport phenomena. Here the effect of acetonitrile (ACN) on the conformational

Assessment of Blood-brain Barrier Permeability by Intravenous Infusion of FITC-labeled Albumin in a Mouse Model of Neurodegenerative Disease.

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Disruption of blood-brain barrier (BBB) integrity is a common feature for different neurological and neurodegenerative diseases. Although the interplay between perturbed BBB homeostasis and the pathogenesis of brain disorders needs further investigation, the development and validation of a reliable

Human serum albumin can regulate amyloid-β peptide fiber growth in the brain interstitium: implications for Alzheimer disease.

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Alzheimer disease is a neurodegenerative disorder characterized by extracellular accumulation of amyloid-β peptide (Aβ) in the brain interstitium. Human serum albumin (HSA) binds 95% of Aβ in blood plasma and is thought to inhibit plaque formation in peripheral tissue. However, the role of albumin

Anti-aggregation properties of trehalose on heat-induced secondary structure and conformation changes of bovine serum albumin.

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During our experimental work, aggregation of bovine serum albumin was obtained incubating the protein solution at 60 degrees C to investigate temperature-induced secondary structure, conformation changes and anti-aggregative activity of trehalose. IR-measurements suggested that in the presence of

Activated microglial cells synthesize and secrete AGE-albumin.

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A holy grail of curing neurodegenerative diseases is to identify the main causes and mechanisms underlying neuronal death. Many studies have sought to identify these targets in a wide variety of ways, but a more important task is to identify critical molecular targets and their origins. Potential

Albumin enhances superoxide production in cultured microglia.

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Microglial activation and disruption of blood-brain barrier (BBB) are known to occur and contribute to neuronal damages in cerebral ischemic conditions and in some neurodegenerative diseases. To investigate whether a serum factor leaked out from circulation enhances microglial activation, we

Pure albumin is a potent trigger of calcium signalling and proliferation in microglia but not macrophages or astrocytes.

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Microglial activation is implicated in the neurotoxicity of neurodegenerative diseases. Raised intracerebral levels of albumin are associated with the pathology of Alzheimer's disease, multiple sclerosis, and stroke where blood-brain barrier damage is evident. We report here that treatment of

Inhibition of Human Serum Albumin Fibrillation by Two-Dimensional Nanoparticles.

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The formation and deposition of amyloid fibrils have been linked to the pathogenesis of numerous debilitating neurodegenerative disorders. Serum albumins serve as good model proteins for understanding the molecular mechanisms of protein aggregation and fibril formation. Graphene-based

Low serum albumin level is risk factor for patients with percutaneous endoscopic gastrostomy.

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OBJECTIVE In Japan, percutaneous endoscopic gastrostomy (PEG) has been used mainly in patients with stroke and dementia, who undertake oral ingestion voluntarily. We have used PEG for patients with various diseases in Saga Medical School Hospital, including postoperative recovery, malignant disease,

Binding of thioflavin T by albumins: An underestimated role of protein oligomeric heterogeneity.

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Amyloid fibrils formation is the well-known hallmark of various neurodegenerative diseases. Thioflavin T (ThT)-based fluorescence assays are widely used to detect and characterize fibrils, however, if performed in bioliquids, the analysis can be biased due to the presence of other, especially

Hydrophobicity alone can not trigger aggregation in protonated mammalian serum albumins.

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Amyloid fibrils are associated with neurodegenerative disorders and are formed by a number of proteins. In this study, the amyloid-forming behavior of several different serum albumins was examined at pH 3.5 i.e., about two pH units below their isoelectric points (pI ∼ 5.5) to examine the roles

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