• All recognized mutations for AD are associated with increased deposition of amyloid-beta (Abeta), a peptide fragment comprising 39-43 amino acids that derive from the catabolism of the amyloid precursor protein (APP) molecule. (medscape.com)
  • iv) Brain cholesterol affects the Aβ formation from amyloid precursor protein (APP) ( 13 , 14 ). (spandidos-publications.com)
  • Aβ is proteolytically cleaved from a large transmembrane amyloid precursor protein (APP) by β and γ secretases[ 3 ]. (biomedcentral.com)
  • To find out, first authors Yuyan Zhu and Huayan Hou crossed PSAPP mice (which overexpress human amyloid precursor protein and presenilin-1 with familial AD-linked mutations) with CD45-knockout mice, and analyzed their progeny at four or eight months of age. (alzforum.org)
  • There was no family history of AD, CJD, or any other neurological disease, and genetic analysis showed no disease specific mutations of the prion protein, presenilin 1 and 2, or amyloid precursor protein genes. (bmj.com)
  • AB40 and AB42 are the two primary forms of amyloid beta that are generated from amyloid precursor protein. (yourbiohealth.com)
  • Active immunization with fibrillar beta-amyloid peptide (AB42) as well as passive transfer of anti-AB antibodies significantly reduces AB plaque deposition, neuritic dystrophy, and astrogliosis in the brain of mutant amyloid precursor protein (APP)-transgenic mice. (ecu.edu)
  • Mutations in genes for the amyloid precursor protein, presenilin I, and presenilin II may lead to autosomal dominant forms of Alzheimer disease, typically with early onset. (msdmanuals.com)
  • Also known as beta-secretase, BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP). (blogspot.com)
  • The plaques mainly consist of beta-amyloid (Aβ) peptides, which are generated through cleavage of the amyloid precursor protein (APP) by secretases, such as beta-site APP-cleavage enzyme 1 (BACE1). (biologists.com)
  • Amyloid plaques contain many proteins in addition to beta amyloid (Aβ). (researchsquare.com)
  • The aim of this study was to comprehensively identify proteins that are enriched in amyloid plaques using unbiased proteomics in two subtypes of early onset AD: sporadic early onset AD (EOAD) and Down Syndrome (DS) with AD. (researchsquare.com)
  • Amyloid plaques and neighbouring non-plaque tissue were microdissected from human brain sections using laser capture microdissection and label-free LC-MS was used to quantify the proteins present. (researchsquare.com)
  • 48 proteins were consistently enriched in amyloid plaques in EOAD and DS. (researchsquare.com)
  • Many of these proteins were more significantly enriched in amyloid plaques than Aβ. (researchsquare.com)
  • The most enriched proteins in amyloid plaques in both EOAD and DS were: COL25A1, SMOC1, MDK, NTN1, OLFML3 and HTRA1. (researchsquare.com)
  • Endosomal/lysosomal proteins were particularly highly enriched in amyloid plaques. (researchsquare.com)
  • Fluorescent immunohistochemistry was used to validate the enrichment of four proteins in amyloid plaques (moesin, ezrin, ARL8B and SMOC1) and to compare the amount of total Aβ, Aβ40, Aβ42, phosphorylated Aβ, pyroglutamate Aβ species and oligomeric species in EOAD and DS. (researchsquare.com)
  • Overall, we observed that amyloid plaques in EOAD and DS largely contained the same proteins, however the amount of enrichment of some proteins was different in EOAD and DS. (researchsquare.com)
  • Our study highlights the significant enrichment of many proteins in amyloid plaques, many of which may be potential therapeutic targets and/or biomarkers for AD. (researchsquare.com)
  • Amyloid plaques are a neuropathological hallmark of Alzheimer's disease and primarily consist of the protein beta amyloid (Aβ). (researchsquare.com)
  • However, it is often overlooked that amyloid plaques also contain hundreds of proteins in addition to Aβ. (researchsquare.com)
  • Therefore, comprehensively profiling the proteins that are enriched in amyloid plaques would increase our understanding about AD pathogenesis, and possibly identify new biomarkers and/or new therapeutic targets for AD. (researchsquare.com)
  • The latter is a neurodegenerative disease, which is characterized by dementia, along with a dense deposition of amyloid-β (Aβ) protein in senile plaques in the brain, hyperphosphorylated tau protein and neuron loss. (spandidos-publications.com)
  • Amyloid beta peptide (Aβ) is the main component of extraneuronal senile plaques typical of Alzheimer's disease (AD) brains. (biomedcentral.com)
  • One of the important hallmarks of AD is the formation of extracellular senile plaques, preferentially composed of amyloid beta-protein[ 1 ]. (biomedcentral.com)
  • The way that amyloid beta (Aß) peptide is deposited into insoluble plaques in Alzheimer's disease is still unknown. (brightfocus.org)
  • There is some evidence that apolipoprotein E (apoE) binds to Aß peptide and modulates its aggregation into plaques. (brightfocus.org)
  • peptide deposition into cerebral senile plaques. (neurodegenerationresearch.eu)
  • Alzheimer's disease is an incurable disorder of the brain characterized by the presence in the brain of protein aggregates called amyloid plaques. (neurodegenerationresearch.eu)
  • This neurodegenerative disorder is characterized by amyloid deposition in senile plaques, composed primarily of fibrils of an aggregated peptide, beta-amyloid. (substack.com)
  • Since the structure of proteins in amyloid plaques are different from the native structure, amyloidogenic proteins must at least partially unfold during amyloidogenesis. (biomedcentral.com)
  • Surprisingly, we found Alzheimer-type senile plaques and cerebral amyloid angiopathy in widespread areas of the brain. (bmj.com)
  • Amyloid beta peptide accumulation in the brain can form extracellular plaques. (yourbiohealth.com)
  • A fundamental feature of AD is brain region-specific deposition of extracellular amyloid plaques principally comprised of the amyloid-β: Aβ) peptide. (wustl.edu)
  • Deposition of the amyloid-beta (A-beta) peptide in the form of amyloid plaques is one of the hallmarks of the disease, occurring early in the development of this condition. (beinghealthyforlife.com)
  • In this project, he is assessing whether proteins that form amyloid plaques may actually be containing the spread of infection from P. gingivalis, which causes gum disease. (eventscribe.net)
  • He will expose mice with the protein and those without it to P. gingivalis to determine if the infection spreads more quickly or more slowly if the protein that forms amyloid plaques is not there. (eventscribe.net)
  • beta-amyloid is the main component of neuritic (senile) plaques, which consist of degenerated axonal or dendritic processes, astrocytes, and glial cells around an amyloid core. (msdmanuals.com)
  • A team of researchers from the Cleveland Clinic Lerner Research Institute have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer's disease, thereby improving the animals' cognitive function. (blogspot.com)
  • One of the earliest events in Alzheimer's disease is an abnormal buildup of beta-amyloid peptide, which can form large, amyloid plaques in the brain and disrupt the function of neuronal synapses. (blogspot.com)
  • The researchers then bred these rodents with mice that start to develop amyloid plaques and Alzheimer's disease when they are 75 days old. (blogspot.com)
  • The characteristic features of AD pathology are amyloid plaques, neurofibrillary tangles and loss of neuronal connections in the brain (1). (biologists.com)
  • Light-sheet microscopy analysis revealed that 6-month-old CNP -/- 5xFAD and PLP1 -/y 5xFAD double mutants exhibited a higher load of amyloid plaques than 5xFAD mice. (biologists.com)
  • Similarly, induction of experimental autoimmune encephalomyelitis (EAE) - a model for chronic immune-mediated myelin loss - caused the formation of amyloid plaques in the spinal cord of 5xFAD mice. (biologists.com)
  • Following its peripheral injection, a fluorescein-labelled version of RI-OR2-TAT was found to cross the blood brain barrier and bind to the amyloid plaques and activated microglial cells present in the cerebral cortex of 17-months-old APPswe/PS1ΔE9 transgenic mice. (derby.ac.uk)
  • The current dogma in the field postulates that the appearance of extracellular amyloid-beta (Aβ) plaques, a histopathological hallmark of the disease, is the trigger for downstream, detrimental events, including neuronal loss, extensive neuroinflammation and cognitive decline. (lu.se)
  • As the kinetics of fibrillation is strongly dependent on the presence of trace amounts of fibrils, we suggest that the aggregation of beta-amyloid is a model of autocatalytic reaction. (substack.com)
  • Accumulation and deposition of amyloid beta peptide (Abeta) within the mind causes neuronal apoptosis and finally results in Alzheimer's illness (AD). (ncbcs.org)
  • In this review, nanowired delivery of cerebrolysin-a balanced composition of several neurotrophic factors and active peptide fragments together with monoclonal antibodies to neuronal nitric oxide synthase (nNOS) with p-tau antibodies was examined in PD following CHI in model experiments. (bvsalud.org)
  • In CALHM1 KO mice, we will first determine whether CALHM1 deficiency affects neuronal integrity and leads to amyloid deposition in the mouse brain. (neurodegenerationresearch.eu)
  • In general, elevated plasma concentrations of these biomarkers are implicated in plaque accumulation and deposition, abnormal phosphorylation and filament bundle aggregation, and neuronal degeneration for overall AD progression. (yourbiohealth.com)
  • We found that ISF Aβ concentrations in several brain regions of APP transgenic mice prior to the onset of plaque deposition were proportional to the degree of subsequent plaque deposition and with the concentration of lactate, a marker of neuronal activity. (wustl.edu)
  • Moreover, we found that physiological modulation of endogenous neuronal activity by vibrissal manipulation was sufficient to modulate ISF Aβ levels and amyloid plaque growth dynamics. (wustl.edu)
  • Together, these data suggest that endogenous neuronal activity and functional connectivity may regulate region-specific Aβ plaque deposition. (wustl.edu)
  • Therefore, we hypothesized that endocannabinoids might reduce amyloid β-protein deposition and inhibit neuronal cell death through CB1 or other possible pathways. (uwaterloo.ca)
  • Apo E proteins influence beta-amyloid deposition, cytoskeletal integrity, and efficiency of neuronal repair. (msdmanuals.com)
  • Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes. (blogspot.com)
  • However, increasing evidence suggests that neuroinflammatory alterations and synaptic and neuronal dysfunction occur already before plaque deposition, which we have also noted in previous work done by our groups. (lu.se)
  • they provide insight into the factors that drive amyloid plaque development and are potential biomarkers or therapeutic targets for Alzheimer's disease (AD). (researchsquare.com)
  • A hallmark of Alzheimer's disease is the brain deposition of amyloid beta (Aβ), a peptide of 36-43 amino acids that is likely a primary driver of neurodegeneration. (rcsb.org)
  • Even one night of sleep deprivation leads to accumulation of amyloid beta peptide burden that would lead to precipitation of Alzheimer's disease over the years. (bvsalud.org)
  • Thus, efforts are needed to slow down or neutralize accumulation of amyloid beta peptide (AßP) and associated Alzheimer's disease brain pathology including phosphorylated tau (p-tau) within the brain fluid environment. (bvsalud.org)
  • We demonstrate the effectiveness of this approach by identifying drug-like, head-to-tail cyclic peptides that modulate the aggregation of the Alzheimer's disease-associated amyloid β peptide. (nature.com)
  • Biochemical, biophysical and biological assays using isolated amyloid β peptide, primary neurons and various established Alzheimer's disease nematode models showed that the selected macrocycles potently inhibit the formation of neurotoxic amyloid β peptide aggregates. (nature.com)
  • The goal of this proposal is to elucidate the exact role played by CALHM1 in amyloid plaque formation and in the progression of Alzheimer's disease. (neurodegenerationresearch.eu)
  • Amyloidogenic proteins are most often associated with neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, but there are more than two dozen human proteins known to form amyloid fibrils associated with disease. (biomedcentral.com)
  • Some of the most well-known amyloidoses are neurodegenerative diseases such as Alzheimer's disease (involving amyloid-beta peptide) and Parkinson's disease (involving alpha-synuclein protein). (biomedcentral.com)
  • Polymorphisms in the promoter region of the apolipoprotein E gene (APOE) affect the amount of amyloid peptide (A beta) in the brains of patients with Alzheimer's disease. (birmingham.ac.uk)
  • We measured A beta load immunohistochemically in regions 8 and 9 of Brodman's area in 74 people with Alzheimer's disease. (birmingham.ac.uk)
  • Alzheimer's disease (AD) and the toxicity and mechanisms of amyloid protein aggregation will be emphasized in this review. (hyperthermicwellness.com)
  • To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models," says Yan, who will be moving to become chair of the department of neuroscience at the University of Connecticut this spring. (blogspot.com)
  • Alzheimer's disease (AD) is a progressive, neurodegenerative disorder characterized by amyloid deposition in the cerebral neuropil and vasculature. (nih.gov)
  • Previously, we have developed a retro-inverso peptide inhibitor (RI-OR2, rGffvlkGr) that blocks the in vitro formation and toxicity of the Aβ oligomers which are thought to be a cause of neurodegeneration and memory loss in Alzheimer's disease. (derby.ac.uk)
  • Our data suggest that oxidative damage, inflammation, and inhibition of neurogenesis are all a downstream consequence of Aβ aggregation, and identify a novel brain-penetrant retro-inverso peptide inhibitor of Aβ oligomer formation for further testing in humans as a potential disease-modifying treatment for Alzheimer's disease. (derby.ac.uk)
  • Neuroinflammation and amyloid-β in early Alzheimer's disease. (lu.se)
  • Dive into the research topics of 'Neuroinflammation and amyloid-β in early Alzheimer's disease. (lu.se)
  • BMI1 knockout in human post-mitotic neurons resulted in amyloid beta peptide secretion and deposition, p-Tau accumulation, and neurodegeneration. (nih.gov)
  • Significance of inflammation-associated regenerative mucosa characterized by Paneth cell metaplasia and beta-catenin accumulation for the onset of colorectal carcinogenesis in rats initiated with 1,2-dimethylhydrazine.Carcinogenesis. (jsvp.jp)
  • Using mouse models of cerebral Aβ deposition, we examined molecular, cellular and systems-level mechanisms that regulate brain region-specific Aβ accumulation and aggregation. (wustl.edu)
  • With the goal of further elucidating some of the processes that drive Alzheimer's progression, new research published in the Nature Partner Journal Aging and Mechanisms of Disease studied the association between A-beta accumulation and the development of neuroinflammation, as well as possible therapeutic interventions. (beinghealthyforlife.com)
  • It is believed that the neuropathogenesis of this disease may be triggered by the accumulation of toxic amyloid in the central nervous system (CNS). (hyperthermicwellness.com)
  • There is evidence that microglia form a protective barrier around amyloid aggregates to prevent further Aβ accumulation (2). (biologists.com)
  • Amyloidoses are a group of diseases defined by the formation of protein aggregates characterized by stacks of cross-beta sheets [ 1 ]. (biomedcentral.com)
  • The formation of toxic aggregates of amyloid-beta-peptide (Abeta), through the activities of beta - and gamma- secretases, is considered as the earlier event in the pathogenesis of the disease. (unicatt.it)
  • Although this copper chelator could possibly interfere with plaque formation, Cuprizone-treated mice showed a substantial increase of amyloid aggregates in regions of strong demyelination. (biologists.com)
  • The Abeta peptide has been found in the brains of children with DS as young as 8 years, and the deposits increase with age. (medscape.com)
  • The deposition of both Abeta and the following hyperphosphorylation of tau protein, trigger an exaggerate immune-inflammatory response culminating with the production of excess reactive oxygen and nitrogen species responsible for damage on cellular nucleic acids, proteins and lipids. (unicatt.it)
  • These amyloid deposits comprise predominantly fragments and full-length (40 or 42 residue) forms of the amyloid beta-protein (Abeta) organized into fibrillar assemblies. (nih.gov)
  • Compelling evidence indicates that factors that increase overall Abeta production or the ratio of longer to shorter forms, or which facilitate deposition or inhibit elimination of amyloid deposits, cause AD or are risk factors for the disease. (nih.gov)
  • Amyloidosis depots contain not only the major fibrillar component but also minor nonfibrillar components such as glycosaminoglycans (GAGs), apolipoprotein E (apoE), and serum amyloid P (SAP) components [ 3 ]. (hyperthermicwellness.com)
  • iii) In a transgenic mouse model of AD (B6Tg2576), early atherosclerosis lesions were detected and were positively correlated with cerebral β amyloid deposits when mice were fed a normal diet ( 11 ) or atherogenic diets ( 12 ). (spandidos-publications.com)
  • Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. (scienceopen.com)
  • Plaque-type and vascular amyloid was immunohistochemically identified as deposits of beta-A4 peptide. (bmj.com)
  • Alzheimer disease causes progressive cognitive deterioration and is characterized by beta-amyloid deposits and neurofibrillary tangles in the cerebral cortex and subcortical gray matter. (msdmanuals.com)
  • amyloid deposits exhibit an apple-green birefringence under a polarized light microscope after staining with the dye Congo red and appear as rigid, nonbranching fibrils 7.5 to 10 nm in diameter under extremely high magnification using an electron microscope [ 5 ]. (hyperthermicwellness.com)
  • Neurofibrillary tangles and the deposition of a beta amyloid peptide with a novel N-terminal epitope in the brains of wild Tsushima leopard cats. (jsvp.jp)
  • Beta -amyloid may also alter kinase and phosphatase activities in ways that eventually lead to hyperphosphorylation of tau (a protein that stabilizes microtubules) and formation of neurofibrillary tangles. (msdmanuals.com)
  • We are interested in the relationship between beta-amyloid deposition and the progressive formation of dystrophic neurites and cell death in hippocampal neurons. (northwestern.edu)
  • VIP treatment has been shown to reduce amyloid-beta deposition, improve learning and memory, and protect neurons from death. (genx.bio)
  • We focused our study on early onset AD as the drivers of the more aggressive pathology development in these cases is unknown and it is unclear whether amyloid-plaque enriched proteins differ between subtypes of early onset AD. (researchsquare.com)
  • A clinical diagnosis of mild cognitive impairment (MCI) due to AD or mild AD dementia, both with confirmed presence of amyloid beta pathology consistent with AD. (cms.gov)
  • Both the isoform and amount of ApoE in the brain modulate AD pathology by altering the extent of amyloid beta (Aβ) peptide deposition. (wustl.edu)
  • investigated the impact of severe reduction of cortical myelin on amyloid pathology. (biologists.com)
  • La estancia postdoctoral que disfruté en el Dementia Research Laboratory (King's College, Londres), me permitió, además de desarrollar mi habilidades técnicas e intelectuales, el ponerme en contacto y comenzar colaboraciones de investigación, que se mantiene a dia de hoy. (unav.edu)
  • In addition to AD, an increasing number of neurodegenerative disorders, including Parkinson's disease, familial British dementia, familial amyloid polyneuropathy, amyotrophic lateral sclerosis, and prion diseases, are associated with abnormal protein assembly processes. (nih.gov)
  • β-sheet breaker peptides inhibit fibrillogenesis in a rat brain model of amyloidosis: implications for Alzheimer's therapy. (nature.com)
  • A progressive increase in amyloid beta peptide deposition is observed, with intracellular immunoreactivity being detected in some brain regions as early as 3-4 months. (mmrrc.org)
  • We also demonstrate a slower turnover rate for CSF ApoE than that for amyloid beta, another molecule critically important in AD pathogenesis. (wustl.edu)
  • The amount of A beta deposition was independent of APOE genotype in our cohort. (birmingham.ac.uk)
  • In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. (scienceopen.com)
  • Potential mechanisms related to overproduction or impaired clearance of these amyloids that may lead to its abnormal deposition in the brain as well as some possible molecular targets for AD treatment will be the focus of this review. (hyperthermicwellness.com)
  • Targeting soluble Aβ peptide with Tramiprosate for the treatment of brain amyloidosis. (nature.com)
  • Amyloidosis is a large group of pathologic conditions in which a particular type of protein, called amyloid, is abnormally deposited in various tissues or organs. (hyperthermicwellness.com)
  • It has been suggested that apoE4 increases amyloid deposition, and it is commonly accepted that the conversion of Aß protein from a soluble form to an insoluble aggregate is associated with a structural or conformational change in the protein. (brightfocus.org)
  • Generally, amyloid refers to misfolded peptides or proteins that demonstrate a stable, cross-beta super-secondary structure that renders it insoluble, fibrous-like, and resistant to proteolysis. (hyperthermicwellness.com)
  • 1) Monoclonal antibodies directed against amyloid that are approved by FDA for the treatment of AD based upon evidence of efficacy from a change in a surrogate endpoint (e.g., amyloid reduction) considered as reasonably likely to predict clinical benefit may be covered in a randomized controlled trial conducted under an investigational new drug (IND) application. (cms.gov)
  • 2) Monoclonal antibodies directed against amyloid that are approved by FDA for the treatment of AD based upon evidence of efficacy from a direct measure of clinical benefit may be covered in CMS approved prospective comparative studies. (cms.gov)
  • In this investigation this hypothesis is examined using nanodelivery of cerebrolysin- a balanced composition of several neurotrophic factors and active peptide fragments together with monoclonal antibodies against AßP, p-tau and serotonin (5-hydroxytryptamine, 5-HT). (bvsalud.org)
  • Using a novel optical intrinsic signal imaging approach, we found that bilateral functional connectivity magnitude in APP/PS1 mice prior to plaque deposition was proportional to the amount of regional plaque deposition in aged APP/PS1 mice. (wustl.edu)
  • assessed amyloid deposition in AD mouse models (5xFAD and APP NLGF , respectively) crossed with mice showing minor structural myelin defects driven by the lack of myelin-proteins like CNP (CNP -/- ) or PLP (PLP -/y ). 5XFAD mice harbor five familial AD (FAD) mutations triggering Aβ overproduction, and already exhibit amyloid deposition two months after birth (4). (biologists.com)
  • To further investigate whether myelin defects can cause plaque deposition, they induced acute demyelination in 5xFAD mice by feeding them Cuprizone. (biologists.com)
  • To see whether these defects stemmed from faulty microglia, the authors stained brain sections with anti-Aβ antibodies and looked to see whether the amyloid clumps also lit up with microglial activation markers (Iba1, CD11b, or CD40), as this would indicate that the phagocytes were reaching their desired target. (alzforum.org)
  • The findings held up in vitro, where CD45-sufficient primary microglia gobbled Aβ peptides faster than did their CD45-deficient counterparts, also in confocal imaging studies, which revealed fluorescent Aβ within the cytoplasm of wild-type microglia but remaining on the surface of CD45-deficient cells. (alzforum.org)
  • 1995). For example, hypertension may lead to cerebral ischemia, which may potentiate aggregation or deposition of amyloid-beta peptides (Aß) through mechanisms such as increased Aß production (Banati et al. (alzrisk.org)
  • So far, there have been a vast number of studies that have hypothesized disease mechanisms for AD, the majority of which support the amyloid hypothesis. (hyperthermicwellness.com)
  • Fibrillation of beta-amyloid is a nucleation-dependent polymerization process, which is controlled by two kinetics parameters: the nucleation rate and the elongation or growth rate. (substack.com)
  • Increasing attention focuses on CSF flow: how it impacts cerebral metabolism and hemodynamics, neural stem cell progression in the subventricular zone, and catabolite/peptide clearance from the CNS. (scienceopen.com)
  • Parallel studies using in vivo multiphoton microscopy and in vivo microdialysis revealed that modest pharmacological reduction of soluble interstitial fluid: ISF) Aβ levels was associated with a dramatic reduction in amyloid plaque formation and growth. (wustl.edu)
  • This indicates that chronic and acute myelin dysfunction trigger amyloid deposition and reveals myelin defects as a risk factor for plaque formation. (biologists.com)
  • Several studies have investigated the role of amyloidogenic mutations on lysozyme amyloid formation with a focus on the first identified mutations, I56T and D67H. (biomedcentral.com)
  • Antibodies bound to the blocking peptide no longer bind to the epitope on the target protein. (affbiotech.com)
  • It has been demonstrated that glucagon-like peptide-1 (GLP-1), which is an endogenous insulinotropic peptide secreted from the intestine, binds to its receptor within the mind and possesses neuroprotective results. (ncbcs.org)
  • Immunohistochemistry showed widespread cortical depositions of disease associated prion protein (PrP sc ) in a synaptic pattern, and western blot analysis identified PrP sc of type 2A according to Parchi et al . (bmj.com)
  • Blood-brain barrier dysfunction could make it possible for brain-reactive autoantibodies to reach the brain, where they can react with amyloid ß peptide (AßP). (immunoscienceslab.com)
  • Fine epitope analysis with overlapping peptides of the AB42 sequence identified the 1- 15 region as a dominant B cell epitope. (ecu.edu)
  • These peptide usually contains the epitope recognized by the antibody. (affbiotech.com)
  • Lysozyme is an antimicrobial protein that is used as a general model to study amyloid fibril formation. (biomedcentral.com)
  • Studies aimed at elucidating the process of amyloid formation of lysozyme tend to focus on partial unfolding of the native state due to the relative instability of mutant amyloidogenic variants. (biomedcentral.com)
  • An analysis of the most energetically favored predicted dimers and trimers provided further evidence for a role for residues 21, 62, 104, 122, and 112-117 in amyloid formation. (biomedcentral.com)
  • Identifying residues in the native state that may be involved in amyloid formation could provide novel drug targets to prevent a range of amyloidoses. (biomedcentral.com)
  • Since lysozyme is structurally and functionally well-characterized, the protein provides a useful model for understanding the complex process of amyloid fibril formation [ 13 ]. (biomedcentral.com)
  • Methylene blue inhibits amyloid Aβ oligomerization by promoting fibrillization. (nature.com)
  • Recombinant expression, in vitro refolding, and biophysical characterization of the human glucagon -like peptide-1 receptor. (ncbcs.org)
  • Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult," says Yan. (blogspot.com)