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> Chemicals & Drugs > Amino Acid > Amyloid

Amyloid

Amyloid is a general term referring to an insoluble fibrous protein material that is deposited in various tissues, often in association with disease.
These fibrils typically have a beta-pleated sheet structure and are resistant to degradation.
Amyloid deposits can lead to disruption of normal tissue structure and function, contributing to a variety of conditions such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes.
Reseach into amyloid and amyloidosis is critical for understanding the mechanisims of these diseeases and developing effective treatments.

Most cited protocols related to «Amyloid»

1
Identifying Gene-Trait Correlations in Alzheimer's Disease
Cited 50 times
First, for each major cell-type, a gene-wise correlation coefficient (Spearman’s rank correlation coefficient) was computed using gene expression and AD-related neuropathological trait values across all the annotated cells as variables. The AD-related neuropathological traits included in this analysis were cogn_global_lv (global cognitive function - last valid score), age_death (age at death), educ (years of education), msex (self-reported sex), parksc_lv (global parkinsonian summary score - last valid score), gpath (global AD pathology burden), gpath_3neocort (global measure of neocortical pathology), pmi (post-mortem interval), amyloid (Overall amyloid level), plaq_d (diffuse plaque burden), plaq_n (neuritic plaque burden), nft (neurofibrillary tangle burden), and tangles (tangle density). Only significant correlations after Bonferroni correction at P<0.01 were considered. The resulting correlation matrices for each major cell-type were concatenated and analyzed using a computational algorithm (self-organizing map, SOM)37 . All SOMs were created using the Kohonen R package56 . To identify the territories of the SOM most strongly correlated with AD-related neuropathological traits, we used an image segmentation method and further manual curation to identify territories (gene-trait correlation modules) based on all the individual cell-type-specific SOM plots for each neuropathological trait. Enrichment analysis for Gene Ontology (GO) terms among the genes of a gene-trait correlation module was performed using Metascape53 . The robustness of gene-trait associations to single-cell heterogeneity and noise was confirmed examining individual-level correlations for the genes in gene-trait module. Individual-level correlations were computed by first averaging for each individual normalized gene expression profiles across cells of the same cell. This resulted in cell-type-specific averaged gene expression profiles across the 48 individuals. Average profiles were subsequently mean-centered and scaled to finally compute gene-wise correlation coefficients versus corresponding pathological values. Individual-level gen-trait correlations were computed independently for all 48 individuals, for only 24 male individuals, and for only 24 female individuals. The robustness of gene-trait associations to potential confounding variables was corroborated by confirming the cell-type specific recovery of identified gene-trait modules using partial correlation. Briefly, the partial Pearson’s correlation coefficient between average gene expression and each pathological trait, after correcting for the effect of PMI, age, gender, and education level of each individual; was computed by first orthogonalizing the normalized expression with respect to the normalized covariates and then computing the correlation in the residual subspace.
Mathys H., Davila-Velderrain J., Peng Z., Gao F., Mohammadi S., Young J.Z., Menon M., He L., Abdurrob F., Jiang X., Martorell A.J., Ransohoff R.M., Hafler B.P., Bennett D.A., Kellis M, & Tsai L.H. (2019). Single-cell transcriptomic analysis of Alzheimer’s disease. Nature, 570(7761), 332-337.
Publication 2019
Amyloid Autopsy Cell Microarray Analysis Cells Cognition Cytosol Females Gene Expression Gene Modules Genes Genetic Heterogeneity Males Neurofibrillary Tangle Senile Plaques
2
Modeling Alzheimer's Disease in iPSC-derived Neurons
Cited 46 times
Primary fibroblast cultures were established from dermal punch biopsies taken from individuals following informed consent and Institutional Review Board approval. To generate iPSCs, fibroblasts were transduced with MMLV vectors containing the complementary DNAs for OCT4, SOX2, KLF4, c-MYC and ± EGFP. IPSC-derived NPCs were differentiated for 3 weeks, neurons were purified by FACS, and amyloid-β, p-tau/total tau and aGSK-3β were measured on purified control and mutant neurons from multiple lines cultured in parallel for an additional 5 days by multi-spot electrochemiluminescence assays (Meso Scale Diagnostics). Early endosomes were analysed by confocal microscopy on purified neurons co-cultured with human astrocytes (Lonza) for 12 days. To ensure reproducible and consistent data, we found that it is important to differentiate and evaluate neurons from full sets of mutant and control iPSC lines together.
Israel M.A., Yuan S.H., Bardy C., Reyna S.M., Mu Y., Herrera C., Hefferan M.P., Van Gorp S., Nazor K.L., Boscolo F.S., Carson C.T., Laurent L.C., Marsala M., Gage F.H., Remes A.M., Koo E.H, & Goldstein L.S. (2012). Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells. Nature, 482(7384), 216-220.
Publication 2012
Amyloid Astrocytes Biological Assay Biopsy Cloning Vectors Diagnosis DNA, Complementary Endocytic Vesicles Ethics Committees, Research Fibroblasts Homo sapiens Induced Pluripotent Stem Cells KLF4 protein, human Microscopy, Confocal Neurons Oncogenes, myc POU5F1 protein, human SOX2 protein, human
3
Modeling Alzheimer's Disease in iPSC-derived Neurons
Cited 43 times
Primary fibroblast cultures were established from dermal punch biopsies taken from individuals following informed consent and Institutional Review Board approval. To generate iPSCs, fibroblasts were transduced with MMLV vectors containing the complementary DNAs for OCT4, SOX2, KLF4, c-MYC and ± EGFP. IPSC-derived NPCs were differentiated for 3 weeks, neurons were purified by FACS, and amyloid-β, p-tau/total tau and aGSK-3β were measured on purified control and mutant neurons from multiple lines cultured in parallel for an additional 5 days by multi-spot electrochemiluminescence assays (Meso Scale Diagnostics). Early endosomes were analysed by confocal microscopy on purified neurons co-cultured with human astrocytes (Lonza) for 12 days. To ensure reproducible and consistent data, we found that it is important to differentiate and evaluate neurons from full sets of mutant and control iPSC lines together.
Israel M.A., Yuan S.H., Bardy C., Reyna S.M., Mu Y., Herrera C., Hefferan M.P., Van Gorp S., Nazor K.L., Boscolo F.S., Carson C.T., Laurent L.C., Marsala M., Gage F.H., Remes A.M., Koo E.H, & Goldstein L.S. (2012). Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells. Nature, 482(7384), 216-220.
Publication 2012
Amyloid Astrocytes Biological Assay Biopsy Cloning Vectors Diagnosis DNA, Complementary Endocytic Vesicles Ethics Committees, Research Fibroblasts Homo sapiens Induced Pluripotent Stem Cells KLF4 protein, human Microscopy, Confocal Neurons Oncogenes, myc POU5F1 protein, human SOX2 protein, human
4
Differential DNA Methylation in Alzheimer's Disease
Cited 19 times
All computations and statistical analyses were performed using R 3.0.242 and Bioconductor 2.1343 (link). Signal intensities were imported into R using the methylumi package44 as a methylumi object. Initial quality control checks were performed using functions in the methylumi package to assess concordance between reported and genotyped gender. Non-CpG SNP probes on the array were also used to confirm that all four brain regions and matched bloods were sourced from the same individual in the London Cohort and two brain regions in the Mount Sinai cohort where expected. Data was pre-processed in the R package wateRmelon using the dasen function as previously described11 (link). Array data for each of the tissues was normalized separately and initial analyses were performed separately by tissue. The effects of age and sex were regressed out before subsequent analysis. For identification of DMPs specifically altered with respect to neuropathological measures of AD, we performed a quantitative analysis where samples were analyzed using linear regression models in respect to Braak stage (London N = 117, Mount Sinai N = 144) and amyloid burden (Mount Sinai N = 144). We used a two-level strategy for avoiding spurious signals due to SNPs rather than DNA methylation differences. Probes with common (MAF > 5%) SNPs in the CG or single base extension position or probes that are nonspecific or mismapped were flagged and disregarded in the evaluation of our results45 (link). In order to also clean up rarer SNPs whilst discarding minimum data, within each tissue, and for each probe, we discarded beta values lying more than four times the interquartile range from the mean; these extreme outliers are generally the result of polymorphisms. Data was analyzed separately in each brain region using linear regression with probes ranked according to P value, and Q-Q plots assessed to check for P value inflation (see Supplementary Fig. S5 for example). To identify differentially methylated regions (DMRs), we identified spatially correlated P values within our data using the Python module comb-p18 (link) to group ≥4 spatially correlated CpGs within a 500bp sliding window. The CETS package in R17 was used to check whether our top-ranked DMPs were mediated by the effect of differential neuronal cell proportions across samples. To identify probes with consistent associations between Braak stage and methylation across the three cortical regions, we employed a meta-analysis of EC, STG and PFC. P values from the individual region results for each site were generated using Fisher’s method and (as a way of controlling for the covariance of the samples which come from the same individuals) Brown’s method. Raw data has been deposited in GEO under accession number GSE43414.
Lunnon K., Smith R., Hannon E., De Jager P., Srivastava G., Volta M., Troakes C., Al-Sarraj S., Burrage J., Macdonald R., Condliffe D., Harries L.W., Katsel P., Haroutunian V., Kaminsky Z., Joachim C., Powell J., Lovestone S., Bennett D.A., Schalkwyk L, & Mill J. (2014). Cross-tissue methylomic profiling strongly implicates a role for cortex-specific deregulation of ANK1 in Alzheimer’s disease neuropathology. Nature neuroscience, 17(9), 1164-1170.
Publication 2014
Amyloid BLOOD Brain Cells Cephalothin Comb Cortex, Cerebral cytidylyl-3'-5'-guanosine Dasen DNA Methylation Genetic Polymorphism Methylation Neurons Python Single Nucleotide Polymorphism Tissues Unithiol Watermelon
5
Comparison of PVC Methods in Amyloid PET
Cited 19 times

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Publication 2014
A-factor (Streptomyces) Amyloid Brain Cloning Vectors factor A Radionuclide Imaging Technique, Dilution Temporal Lobe Tissues

Most recents protocols related to «Amyloid»

1
Retrospective Analysis of AL Amyloidosis
A consecutive series of 142 newly diagnosed AL amyloidosis patients, who presented to our hospital from November 2012 to December 2021, were analyzed retrospectively. A total of 80 of the 142 newly diagnosed AL amyloidosis patients had primary AL amyloidosis, and the other 62 patients were AL amyloidosis patients with concurrent MM. The diagnosis of AL amyloidosis was confirmed by a Congo-red-positive biopsy and immunohistochemistry of the amyloid [1 (link)]. Meanwhile, the presence of the kappa or lambda chain was confirmed through immunohistochemistry and/or immunofluorescence. Moreover, monoclonal plasma cell proliferation was investigated by multi-color flow cytometry on aspirated bone marrow cells. Patients were evaluated for the presence of symptomatic MM based on the International Myeloma Working Group (IMWG) criteria [11 (link)]: bone marrow clonal plasma cells > 10% and evidence of myeloma-defining events, including the slim-CRAB criteria. Patients with AL amyloidosis with >10% bone marrow plasma cells and any myeloma-defining events were described with coexistent MM. iFISH was performed for all the patients as part of their routine clinical testing. Patients gave written informed consent for the iFISH and data analysis in accordance with the Declaration of Helsinki. Approval was obtained by the Ethics Committee of Shanghai Changzheng Hospital.
Among the 80 primary AL amyloidosis patients, 71 patients were treated with bortezomib-based regimens (cyclophosphamide/bortezomib/dexmethasome (CBd) or bortezomib/dexamethasone (Vd)), five patients treated with lenalidomide-based regimens (lenalidomide/cyclophosphamide/dexmethasome (RCd) or lenalidomide/dexmethasome (Rd)), three patients were treated with thalidomide-based regimens (thalidomide/ cyclophosphamide/dexmethasome (TCd)), and one patient was treated with ixazomib-based regimens (ixazomib/dexmethasome (Id)) for induction therapy, and three of the 80 patients received autologous transplants as a consolidation therapy. Among the 62 AL amyloidosis patients with concurrent MM, 47 patients were treated with bortezomib-based regimens (CBd or Vd), seven patients were treated with lenalidomide-based regimens (RCd or Rd), five patients were treated with bortezomib combined with lenalidomide (bortezomib/lenalidomide/dexmethasome (VRd)), and three patients were treated with daratumumab-based regimens (daratumumab/bortezomib/dexmethasome (DVd)). A total of six of the 62 patients received autologous transplants as a consolidation therapy. None of the 142 patients received venetoclax.
He H., Lu J., Qiang W., Liu J., Liang A, & Du J. (2023). The Landscape of Cytogenetic Aberrations in Light-Chain Amyloidosis with or without Coexistent Multiple Myeloma. Journal of Clinical Medicine, 12(4), 1624.
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Publication 2023
Amyloid Autografts Biopsy Bone Marrow Cells Bortezomib Brachyura Cell Proliferation Clone Cells Cyclophosphamide daratumumab Dexamethasone Diagnosis Ethics Committees, Clinical Flow Cytometry Immunofluorescence Immunohistochemistry ixazomib Lenalidomide Multiple Myeloma Neoadjuvant Therapy Patients Plasma Primary Amyloidosis Thalidomide Therapeutics Treatment Protocols venetoclax
2
Comprehensive Neurodegeneration Biomarker Panel
Primary antibodies against β-secretase (BACE, Cat# 5606), phospho-Tau (p-Tau, Cat# 15013), Tau (Cat# 46687), Catalase (Cat# 12980), NOD-like receptor (NLR) family pyrin domain containing 3 (NLRP3, Cat# 13158), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC, Cat# 67824), Caspase-1 (Cat# 3866), Bcl-2-associated X protein (Bax, Cat# 2772), B-cell lymphoma 2 (Bcl-2, Cat# 3498), cleaved caspase-9 (Cat# 20750), cleaved caspase-3 (Cat# 9664), cleaved poly (ADP-ribose) polymerase (PARP, Cat# 5625), FUN14 Domain-Containing 1 (FUNDC1, Cat# 49240), PTEN-induced putative kinase 1 (PINK1, Cat# 6946), Parkin (Cat# 4211), Beclin1 (Cat# 3495), microtubule-associated protein 1A/1B-light chain 3B (LC3B, Cat# 3868), p-cAMP response element-binding (p-CREB, Cat# 9198), CREB (Cat# 9197), choline acetyltransferase (ChAT, Cat# 27269), p-extracellular signal-regulated kinase (p-ERK, Cat# 4377), ERK (Cat# 4695), and β-actin (Cat# 8457) were obtained from Cell Signaling Technology (Danvers, MA, USA). Superoxide dismutase-1 (SOD-1, Cat# sc-515404), SOD-2 (Cat# sc-137254), β-amyloid (Aβ1–42, Cat# sc-28365), glutathione peroxidase-1 (GPx-1, Cat# sc-133160), glutathione reductase (GR, Cat# sc-133245), and acetylcholinesterase (AChE, Cat# sc-373901) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Nitric oxide synthase (iNOS, Cat# PA1-036) was obtained from Invitrogen Life Technologies (Carlsbad, CA, USA). Tumor necrosis factor α (TNFα, Cat# ab66579), IL-6 (Cat# ab9324), interleukin-1β (IL-1β, Cat# ab9722), and anti-brain-derived neurotrophic factor (BDNF, Cat# ab108319) were purchased from Abcam Inc. (Cambridge, CA, USA). Horseradish peroxidase (HRP)-linked anti-rabbit IgG and HRP-linked anti-mouse IgG antibodies were purchased from GenDEPOT (Barker, TX, USA).
Kim H.L., Lee S.K., Min D.E., Bastola T., Chang B.Y., Bae J.H, & Lee D.R. (2023). Effects of Scrophularia buergeriana Extract (Brainon®) on Aging-Induced Memory Impairment in SAMP8 Mice. Current Issues in Molecular Biology, 45(2), 1287-1305.
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Publication 2023
Acetylcholinesterase Actins Amyloid anti-IgG Antibodies Apoptosis B-Cell Lymphomas Bax Protein BCL2 protein, human BECN1 protein, human Caspase 1 Caspase 3 Caspase 9 Caspase Activation and Recruitment Domain Catalase Choline O-Acetyltransferase Extracellular Signal Regulated Kinases Glutathione Peroxidase GPX1 Glutathione Reductase Horseradish Peroxidase IL1B protein, human Interleukin-1 beta microtubule-associated protein 1B Mus Neurotrophic Factor, Brain-Derived Nitric Oxide Synthase NLR Proteins NOS2A protein, human Pain PARK2 protein, human PARP1 protein, human Phosphorus Phosphotransferases Proteins PTEN protein, human Pyrin Domain Rabbits Secretase Superoxide Dismutase-1 TNF protein, human TNFSF14 protein, human
3
Plasma Amyloid Biomarker Analysis in Alzheimer's
Data were analyzed using the R statistical software (version 4.0.2) [27 ]. For each group, quantitative variables were expressed as the median with the interquartile range (IQR, Q1 and Q3). Groups were compared using non-parametric Kruskal–Wallis or Mann–Whitney tests according to the group number. Pairwise comparisons were adjusted with Bonferroni correction. Correlations were assessed using Spearman’s rank correlation coefficient (ρ). The distribution of categorical variables was expressed with percentages and compared using Fisher’s exact test.
For comparisons of biomarker concentrations between diagnosis groups, to avoid the influence of extreme values, outliers were identified using Rosner’s test and discarded (n = 6). For each group, normal distribution was assessed using the Shapiro–Wilk test and homoscedasticity through Levene’s test. The assumption of normality was not obtained in only two groups, IPMS-Shim and Simoa Aβ42/40 for the AD diagnosis. ANCOVA’s assumptions of linearity, homogeneity of variance, non-collinearity of the factors (variance inflation factor <5), non-influential observations, and normality of residuals were evaluated. The impact of diagnosis on plasma amyloid biomarker concentrations was evaluated using ANCOVA controlling for age and APOE ε4 status. Multiple comparisons of the means were achieved using Tukey contrasts with diagnosis as a factor.
Plasma cutoffs were computed using expectation–maximization (EM) algorithms for mixtures of univariate normal distributions [28 ]. Cutoffs were visually determined at the intersection of two normal distributions.
A receiver operating characteristic (ROC) analysis was used to determine biomarker performances. A predictive formula adjusted for age and APOE ε4 status was built using a logistic regression analysis. The best values for sensitivity (se) and specificity (sp) were computed at an optimal cutoff point. Youden’s index was used to determine this optimal cutoff corresponding to the threshold maximizing the distance to the identity (diagonal) line and giving and equal weight to sensitivity and specificity. The area under the curve (AUC) was compared using the DeLong test. All tests were two-tailed, and significance was set at α = .05.
Hirtz C., Busto G.U., Bennys K., Kindermans J., Navucet S., Tiers L., Lista S., Vialaret J., Gutierrez L.A., Dauvilliers Y., Berr C., Lehmann S, & Gabelle A. (2023). Comparison of ultrasensitive and mass spectrometry quantification of blood-based amyloid biomarkers for Alzheimer’s disease diagnosis in a memory clinic cohort. Alzheimer's Research & Therapy, 15, 34.
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Publication 2023
Amyloid ApoE protein, human Biological Markers Contrast Media Diagnosis Factor V Plasma SHIMS
4
Cytokine Profiling in CSF after Lenalidomide Therapy
CSF samples were collected from participants. They were centrifuged immediately and the supernatant was stored at − 80 °C until testing. The concentration of cytokines in blood was determined by a magnetic bead-based multiplex panel (Luminex™; Bio-Rad Laboratories, Hercules, CA, USA). In 14 patients, levels of the following cytokines in CSF were evaluated: TNF-α, IFN-γ, IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-6, IL-8, IL-10, IL-12p40, IL-12p70, IL-13, IL-17A, interferon-gamma induced protein 10, monocyte chemotactic protein-1, macrophage inflammatory protein (MIP)-1α, MIP-1β, G-CSF, granulocyte–macrophage colony-stimulating factor, soluble CD40 ligand, complement C3, complement factor H (CFH), fibroblast growth factor-2, platelet-derived growth factor-AA, growth-related oncogene, alpha 2-macroglobulin (α2M), apolipoprotein AI (Apo AI), apolipoprotein E (Apo E), amyloid beta 1–42, total tau, and phosphorylated tau. Cytokine concentrations were expressed in pg/mL and determined before and after lenalidomide therapy (refer to Additional file 1: Table S2 for explanation of abbreviations).
Wan Z., Tao R., Hui J., Liu X., Peng X., Guo Y., Zhu X., Huang Y, & Zhu B. (2023). Efficacy and safety of lenalidomide in HIV-associated cryptococcal meningitis patients with persistent intracranial inflammation: an open-label, single-arm, prospective interventional study. Journal of Neuroinflammation, 20, 38.
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Publication 2023
alpha 2-Glucoproteins Amyloid Apolipoprotein A-I Apolipoproteins E BLOOD CCL3 protein, human CCL4 protein, human CD40 Ligand Complement 3 Complement factor H Cytokine Fibroblast Growth Factor 2 Granulocyte-Macrophage Colony-Stimulating Factor Granulocyte Colony-Stimulating Factor IL10 protein, human Interferon Type II Interleukin-1 beta Interleukin-12 Interleukin-12 Subunit p40 Interleukin-13 Interleukin-17A Lenalidomide Monocyte Chemoattractant Protein-1 Oncogenes Patients PDGF AA Proteins Therapeutics Tumor Necrosis Factor-alpha
5
Autologous SCT in Hematologic Cancers
The Korea University bone marrow transplantation registry is a longitudinal cohort containing data of patients who underwent SCT at the Korea University Medical Center (Korea University Anam, Guro, and Ansan Hospitals) from January 2007 to December 2018. According to this registry, 201 patients underwent auto-SCT: 107 with multiple myeloma; 50 with B-cell lymphoma; 35 with T-cell lymphoma; 8 with Hodgkin lymphoma, and 1 with amyloid light-chain (AL) amyloidosis. Patients with AL amyloidosis were excluded because critical medical data were missing. Of the 200 patients, 50 were not tested for CMV reactivation. Thus, we retrospectively analyzed data from 150 patients with multiple myeloma (n = 80), B-cell lymphoma (n = 39), T-cell lymphoma (n = 26), and Hodgkin lymphoma (n = 5). All methods were performed in accordance with relevant guidelines and regulations. This study was approved by the Institutional Review Board of the Korea University Medical Center, with a waiver of informed consent for the collection and analysis of retrospective data.
Lee B.H., Jeon M.J., Yu E.S., Kang K.W., Kim D.S., Lee S.R., Park Y., Sung H.J., Choi C.W, & Kim B.S. (2023). Prognostic outcomes of cytomegalovirus reactivation after autologous stem cell transplantation. International Journal of Medical Sciences, 20(2), 186-193.
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Publication 2023
Amyloid Amyloidosis B-Cell Lymphomas Bone Marrow Transplantation Ethics Committees, Research Hodgkin Disease Light Multiple Myeloma Patients T-Cell Lymphoma

Top products related to «Amyloid»

1
Fetal bovine serum (fbs) by Thermo Fisher Scientific
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Ultrascan 1000 2k 2k ccd camera by Ametek
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The UltraScan 1000 is a 2k×2k CCD camera designed for laboratory applications. It features a high-resolution sensor capable of capturing detailed images. The camera's core function is to provide high-quality image data for scientific analysis and documentation purposes.
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Thioflavin t tht dye by Merck Group
Thioflavin T (ThT) is a fluorescent dye commonly used in research applications. It exhibits enhanced fluorescence upon binding to amyloid fibrils, making it a useful tool for detecting and studying protein aggregation.
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L glutamine by Thermo Fisher Scientific
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Ultrapure grade tht by AnaSpec
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More about "Amyloid"

Amyloid is a general term referring to an insoluble, fibrous protein material that is deposited in various tissues, often in association with disease.
These amyloid fibrils typically have a beta-pleated sheet structure and are resistant to degradation.
Amyloid deposits can lead to disruption of normal tissue structure and function, contributing to a variety of conditions such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes.
Researching amyloid and amyloidosis is critical for understanding the mechanisms of these diseases and developing effective treatments.
PubCompare.ai can enhance amyloid research by helping users find the most effective protocols and products.
Its AI-driven comparisons analyze data from literature, preprints, and patents, ensuring reproducibility and accuracy.
This allows researchers to experience smarter, more efficient amyloid research.
When studying amyloid, researchers may utilize a variety of tools and techniques.
Fluorescence-based Spectroscopy (FBS) and Fluorescence Visiometry (FV3000) can be used to analyze the structural and morphological properties of amyloid fibrils.
Methylcellulose and the UltraScan 1000 (2k×2k) CCD camera can also be employed in amyloid research.
The Thioflavin T (ThT) dye is a common fluorescent probe used to detect and quantify amyloid aggregates, while L-glutamine may be used as a nutrient source for cell cultures.
Microplate readers are often utilized to measure fluorescence or absorbance in amyloid assays, and Quantitative real-time PCR can be used to study gene expression related to amyloid formation.
Ultrapure grade ThT and the compound ZLN005 may also be relevant to amyloid research and therapeutics.