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70 results for “Aβ”
Computational Investigation of Co-Aggregation and Cross-Seeding between Aβ and hIAPP Underpinning the Crosstalk in Alzheimer's Disease and Type-2 Diabetes
<p><span>The coexistence of Amyloid-β (Aβ) and human Islet Amyloid Polypeptide (hIAPP) in the brain and pancreas is associated with an increased risk of Alzheimer’s disease (AD) and type-2 diabetes (T2D) due to their co-aggregation and cross-seeding. Despite this, the molecular mechanisms underlying their interaction remain elusive. Here, we systematically investigated the cross-talk between Aβ and hIAPP using atomistic discrete molecular dynamics (DMD) simulations. Our results revealed that the amyloidogenic core regions of both Aβ (Aβ<sub>10–21</sub> and Aβ<sub>30–41</sub>) and hIAPP (hIAPP<sub>8-20</sub> and hIAPP<sub>22-29</sub>), driving their self-aggregation, also exhibited a strong tendency for cross-interaction. This propensity led to the formation of β-sheet-rich hetero-complexes, including potentially toxic β-barrel oligomers. The formation of Aβ and hIAPP hetero-aggregates did not impede the recruitment of additional peptides to grow into larger aggregates. Our cross-seeding simulations demonstrated that both Aβ and hIAPP fibrils could<a name="_Hlk163119646"></a> mutually act as seeds, assisting each other's monomers in converting into β-sheets at the exposed fibril elongation ends. The amyloidogenic core regions of Aβ and hIAPP, in both oligomeric and fibrillar states, exhibited the ability to recruit isolated peptides, thereby extending the β-sheet edges, with limited sensitivity to the amino acid sequence. These findings suggest that targeting these regions by capping them with amyloid-resistant peptide drugs may hold potential as a therapeutic approach for addressing AD, T2D, and their co-pathologies.</span></p>
Supplemental data for: A bibliometric assessment of the incidence of amyloid-Eszett (Aß), a false positive of amyloid-beta (Aβ), in the neurodegenerative disease literature
<p>One claimed reason for the development of Alzheimer’s disease (AD), a prominent neurodegenerative disease, is the extracellular aggregation of amyloid-beta (Aβ). A linguistic or formatting error has resulted in the misrepresentation of the Greek letter β with the German letter Eszett (ß), resulting in the formation of a non-existent compound, amyloid-Eszett (Aß). These datasets offer a quantified appreciation of the AD-related literature, carrying a mention of this false positive in the title, abstract and keywords of papers indexed in the Web of Science Core Collection and Scopus. Also, as a curiosity given the popularity of this large language model, we asked the questions to ChatGPT. This AI chatbot developed by OpenAI was able to recognize Eszett as a linguistic or typographic error, within this context, recognizing Aß and Aβ as equals. This erroneous substitution of a Greek letter (in Aβ) by a German one (Aß), despite giving a non-existent compound, will likely not change the underlying scientific conclusions of the affected papers, although errata might be useful to enlighten others, including metadata managers and journal copyeditors, so as not to repeat the same mistake.</p>
Data from: A qualitative analysis of an Aβ-monomer model with inflammation processes for Alzheimer's disease
<p>We introduce and study a new model for the progression of Alzheimer's disease incorporating the interactions of Aβ-monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. In order to understand the complete interactions between these elements, we study a spatially-homogeneous simplified model that allows to determine the effect of key parameters such as degradation rates in the asymptotic behavior of the system and the stability of equilibriums. We observe that inflammation appears to be a crucial factor in the initiation and progression of Alzheimer's disease through a phenomenon of hysteresis, which means that there exists a critical threshold of initial concentration of interleukins that determines if the disease persists or not in the long term. These results give perspectives on possible anti-inflammatory treatments that could be applied to mitigate the progression of Alzheimer's disease. We also present numerical simulations that allow to observe the effect of initial inflammation and concentration of monomers in our model.</p>
Data from: A qualitative analysis of an Aβ-monomer model with inflammation processes for Alzheimer’s disease
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Dietary vitamin A modifies the gut microbiota and intestinal tissue transcriptome, impacting intestinal permeability and the release of inflammatory factors, thereby influencing Aβ pathology
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Dataset related to article "Intracerebral Injection of Extracellular Vesicles from Mesenchymal Stem Cells Exerts Reduced Aβ Plaque Burden in Early Stages of a Preclinical Model of Alzheimer's Disease."
<p>Bone marrow Mesenchymal Stem Cells (BM-MSCs), due to their strong protective and anti-inflammatory abilities, have been widely investigated in the context of several diseases for their possible therapeutic role, based on the release of a highly proactive secretome composed of soluble factors and Extracellular Vesicles (EVs). BM-MSC-EVs, in particular, convey many of the beneficial features of parental cells, including direct and indirect β-amyloid degrading-activities, immunoregulatory and neurotrophic abilities. Therefore, EVs represent an extremely attractive tool for therapeutic purposes in neurodegenerative diseases, including Alzheimer's disease (AD). We examined the therapeutic potential of BM-MSC-EVs injected intracerebrally into the neocortex of APPswe/PS1dE9 AD mice at 3 and 5 months of age, a time window in which the cognitive behavioral phenotype is not yet detectable or has just started to appear. We demonstrate that BM-MSC-EVs are effective at reducing the Aβ plaque burden and the amount of dystrophic neurites in both the cortex and hippocampus. The presence of Neprilysin on BM-MSC-EVs, opens the possibility of a direct β-amyloid degrading action. Our results indicate a potential role for BM-MSC-EVs already in the early stages of AD, suggesting the possibility of intervening before overt clinical manifestations.</p>
MD data for the article "Structure comparison of beta amyloid peptide Aβ 1-42 isoforms. Molecular dynamics modeling" by Anna P. Tolstova, Alexander A. Makarov, Alexei A. Adzhubei.
<p>There are CMD and REMD trajectories for Aβ isoforms discussed in the paper together with final coordinate files for these trajectories. The resulting dataset of modeled structures includes wild type Aβ42, isoD7, pS8, D7H and H6R-Aβ42, and wild type Aβ16, isoD7, pS8, D7H and H6R-Aβ16.</p>
A Study to Evaluate the Pharmacodynamic Effects of Single Oral Doses of PF-06648671 on β-Amyloid (Aβ) Concentrations in Cerebrospinal Fluid (CSF)
ClinicalTrials.gov study NCT02407353. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Beta Amyloid PET/CT in Various Aβ-Related Disease
ClinicalTrials.gov study NCT06725706. IPD Sharing: NO. Countries: 1. Publications: 1.
Retinal Nerve Fiber Layer Thickness and Cerebrospinal Fluid Aβ/Tau
ClinicalTrials.gov study NCT03447613. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
Effects of Sleep Deprivation on Cerebrospinal Fluid (CSF) Amyloid-beta (Aβ) Dynamics
ClinicalTrials.gov study NCT01194713. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Multiple Dose Study of Aducanumab (BIIB037) (Recombinant, Fully Human Anti-Aβ IgG1 mAb) in Participants With Prodromal or Mild Alzheimer's Disease
ClinicalTrials.gov study NCT01677572. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Education is associated with Aβ burden in preclinical familial and sporadic Alzheimer’s disease
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Data from: Associations between tau, Aβ, and cortical thickness with cognition in Alzheimer disease
Objective To examine the cross-sectional associations between regional tau, β-amyloid (Aβ), and cortical thickness and neuropsychological function across the preclinical and clinical spectrum of Alzheimer disease (AD). Methods We included 106 participants from the Swedish Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably (BioFINDER) study, of whom 33 had preclinical AD (Aβ-positive cognitively normal individuals), 25 had prodromal AD (Aβ-positive mild cognitive impairment), and 48 had probable AD dementia. All underwent [18F]flortaucipir (tau) and structural MRI (cortical thickness), and 88 of 106 underwent [18F]flutemetamol (Aβ) PET. Linear regression models adjusted for age, sex, and education were performed to examine associations between 7 regions of interest and 7 neuropsychological tests for all 3 imaging modalities. Results In preclinical AD, [18F]flortaucipir, but not [18F]flutemetamol or cortical thickness, was associated with decreased global cognition, memory, and processing speed (range standardized β = 0.35–0.52, p < 0.05 uncorrected for multiple comparisons). In the combined prodromal AD and AD dementia group, both increased [18F]flortaucipir uptake and reduced cortical thickness were associated with worse performance on a variety of neuropsychological tests (most regions of interest survived correction for multiple comparisons at p < 0.05), while increased [18F]flutemetamol uptake was specifically associated with lower scores on a delayed recall memory task (p < 0.05 uncorrected for multiple comparisons). The strongest effects for both [18F]flortaucipir and cortical thickness on cognition were found in the lateral and medial parietal cortex and lateral temporal cortex. The effect of [18F]flutemetamol on cognition was generally weaker and less region specific. Conclusion Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. Furthermore, both [18F]flortaucipir PET and cortical thickness show strong cognitive correlates at the clinical stages of AD.
Specific mutations in the cholesterol-binding site of APP alter its processing and favor the production of shorter, less toxic Aβ peptides.
<p>Mass Spectrometry data of Abeta secreted peptides from HEK293 stable clones expressing APP or APPK28A treated or not with methylbetacyclodextrin-cholesterol.</p>
Data from: Distinct association between APOE ε2 and Aβ in Alzheimer- and vascular-type cognitive impairment
<p><b>Objective:</b> To investigate the association between apolipoprotein E<i> </i>(<i>APOE</i>) genotype and amyloid-β (Aβ) burden, as measured by PET in patients with subcortical vascular cognitive impairment (SVCI) and those with Alzheimer's disease-related cognitive impairment (ADCI).</p> <p><b>Methods:</b> This was a cross-sectional study of 310 patients with SVCI and 999 with ADCI. To evaluate the effects of <i>APOE</i> genotype or diagnostic group on Aβ-positivity, we performed multivariate logistic regression analyses. Further distinctive underlying features of latent subgroups were examined by employing a latent class cluster analysis approach.</p> <p><b>Results: </b>In comparison with ε3 homozygotes, in the ADCI group, ε2 carriers showed a lower frequency of Aβ-positivity (odds ratio [OR] 0.43, 95% CI 0.23–0.79) while in the SVCI group, ε2 carriers showed a higher frequency of Aβ-positivity (OR 2.26, 95% CI 1.02–5.01). In particular, we observed an interaction effect of ε2 carrier status and diagnostic group on Aβ-positivity (OR 5.12, 95% CI 1.93–13.56), in that relative to ε3 homozygotes, there were more Aβ-positive ε2 carriers in the SVCI group than in the ADCI group. We also identified latent subgroups of Aβ-positive <i>APOE</i> ε2 carriers with SVCI and Aβ-positive <i>APOE</i> ε4 carriers with ADCI.</p> <p><b>Conclusions: </b>Our findings suggest that <i>APOE</i> ε2 shows distinctly associated with Aβ deposition in patients with SVCI and those with ADCI. Our findings further suggest that there is a distinctive subgroup of Aβ-positive <i>APOE</i> ε2 carriers with SVCI among patients with cognitive impairments.</p>
Derivation and utility of an Aβ-PET pathology accumulation index to estimate Aβ load
<p><b>Abstract</b></p> <p><b>Objective: </b>To evaluate a novel Aβ-PET based quantitative measure (Aβ accumulation index [Aβ-index]), including the assessment of its ability to discriminate between subjects based on Aβ-status using visual-read, CSF Aβ42/Aβ40 and <i>post-mortem</i> neuritic-plaque burden as standards of truth.</p> <p><b>Methods: </b>1121 subjects (with and without cognitive impairment) scanned with Aβ-PET: Swedish BioFINDER, n=392, [<sup>18</sup>F]flutemetamol; ADNI, n=692, [<sup>18</sup>F]florbetapir; a phase-3 end-of-life study, n=100, [<sup>18</sup>F]flutemetamol). The relationships between Aβ-index and standardized uptake values ratios (SUVR) from Aβ-PET were assessed. The diagnostic performance of Aβ-index and SUVR were compared when using visual reads, CSF Aβ42/Aβ40 and Aβ-histopathology as reference standards.</p> <p><b>Results:</b> Strong associations were observed between Aβ-index and SUVR (R<sup>2</sup>, BioFINDER, 0.951; ADNI, 0.943, end-of-life, 0.916). Both measures performed equally well in differentiating Aβ-positive from Aβ-negative subjects, with AUCs of 0.979-0.991 to detect abnormal visual reads, AUCs of 0.961-0.966 to detect abnormal CSF Aβ42/40 and AUCs of 0.820-0.823 to detect abnormal Aβ-histopathology. Both measures also showed a similar distribution across <i>post-mortem </i>based Aβ-phases (based on anti-Aβ 4G8 antibodies). By comparison to models using visual-read alone, the addition of the Aβ-index resulted in a significant increase in AUC and a decrease in Akaike information criterion to detect abnormal Aβ-histopathology.</p> <p><b>Conclusions</b><b>:</b> The proposed Aβ-index showed a tight association to SUVR and carries an advantage over the latter in that it does not require the definition of regions of interest nor the use of MRI. Aβ-index may thus prove simpler to implement in clinical settings and may also facilitate the comparison of findings using different Aβ-PET tracers.</p>
Derivation and utility of an Aβ-PET pathology accumulation index to estimate Aβ load
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Data from: Distinct association between APOE ε2 and Aβ in Alzheimer- and vascular-type cognitive impairment
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Data from: Associations between tau, Aβ, and cortical thickness with cognition in Alzheimer disease
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.