How to engineering Beta-Amyloid for Alzheimer disease?
Best insight from top research papers
Engineering Beta-Amyloid for Alzheimer's disease involves exploring novel structures like two-dimensional covalent organic frameworks (COFs) , MBenes such as Cd2B, Mo2B, Cu2B, and Ta2B , and stable alginate microbeads containing amyloid-producing cells . These structures have shown potential in preventing Beta-Amyloid aggregation, destabilizing amyloid structures, and providing a platform for studying chronic Aβ production. The use of engineered COFs with amine functional groups and high contact areas can inhibit Beta-Amyloid aggregation and enhance diffusivity through the blood-brain barrier . Similarly, MBenes, especially Cd2B, have demonstrated effectiveness in destabilizing amyloid-β structures, potentially preventing accumulation . Additionally, alginate microbeads encapsulating amyloid-secreting cells offer a stable platform for sustained Aβ release, enabling the modeling of Alzheimer's disease progression in vitro and in vivo .
Answers from top 5 papers
More filters
| Papers (5) | Insight |
|---|---|
| Beta-Amyloid can be engineered for Alzheimer's disease research by utilizing synthetic, cell-derived, brain-derived, or recombinant forms to model Aβ aggregation, neurotoxicity, and cognitive impairment in vitro and in vivo. | |
2 Citations | Encapsulate amyloid-secreting cells in alginate microbeads to model Alzheimer's disease progression, enabling chronic and sustained release of Beta-Amyloid for in vitro and in vivo studies. |
31 Oct 2022 | An efficient method for expressing and purifying Amyloid-Beta (Aβ1-42) peptide from E. coli is optimized, providing a reproducible yield for studying Alzheimer's disease pathology. |
18 Citations | Amine-functionalized COFs with large surface area prevent beta-amyloid aggregation, inhibit protofibril self-assembly, and enhance diffusivity through the blood-brain barrier, showing promise for Alzheimer's disease treatment. |
5 Citations | Novel bioengineered MBenes like Cd2B show promise in destabilizing Beta-amyloid structures, potentially preventing their accumulation in Alzheimer's disease, as per the in-silico study findings. |
Related Questions
How do current engineering techniques target beta-amyloid inhibition?5 answersCurrent engineering techniques target beta-amyloid inhibition through various approaches. One method involves utilizing two-dimensional covalent organic frameworks (COFs) functionalized with amines to prevent beta-amyloid aggregation by inhibiting protofibril self-assembly and creating instability in amyloid structures. Another technique involves the molecular tweezer CLR01, which selectively binds lysine and arginine residues in Aβ peptides, disrupting inter- and intramolecular interactions and reducing β-sheet content in Aβ dimers. Additionally, peptide inhibitors designed based on Aβ fibril structures show promise in selectively recognizing different Aβ species, offering a potential avenue for developing potent amyloid inhibitors for therapeutic purposes. These innovative engineering strategies provide insights into novel approaches for combating Alzheimer's disease by targeting beta-amyloid inhibition.
What are advancements in engineering Beta-Amyloid for Alzheimer disease?5 answersEngineering Beta-Amyloid for Alzheimer's disease has seen advancements through various approaches. Studies have explored utilizing two-dimensional covalent organic frameworks (COFs) to prevent Beta-Amyloid aggregation, showing potential in inhibiting protofibril self-assembly and fibrillation. Additionally, novel structures based on MBenes like Cd2B have demonstrated effectiveness in destabilizing Beta-Amyloid structures, paving the way for potential medicinal agents to prevent amyloid-β accumulation. Furthermore, research on transgenic mouse models has led to the development of App knock-in mice, providing insights into Aβ metabolism, clearance, and the differential roles of enzymes involved in Aβ degradation. These advancements offer promising avenues for future experimental research and therapeutic strategies in combating Alzheimer's disease.
How to model alzheimers in zebra fish?4 answersTo model Alzheimer's disease (AD) in zebrafish, researchers can induce AD-like conditions using agents like Okadaic acid (OKA) to mimic key pathological features. Zebrafish offer a valuable model due to their behavioral patterns, genetic similarities, and sensitivity to neurotropic drugs, allowing for the establishment of behavioral and transgenic AD models. By combining various methods of AD induction in adult zebrafish, a holistic model expressing characteristic AD features can be created for studying the disease's pathogenesis and screening potential drugs. Zebrafish's well-conserved nervous system and established genome make them an excellent comparative model for investigating AD-related behaviors and molecular mechanisms, emphasizing the need for integrating behavioral and transgenic models for comprehensive AD screening. Zebrafish's unique tissue regenerative ability further enhances their utility in early drug discovery and preclinical studies for AD.
How to make mice suffer from alzheimer's?5 answersTo induce Alzheimer's disease (AD) in mice, researchers have utilized various methods. One approach involves intracerebroventricular (ICV) injection of streptozotocin (STZ), a diabetogenic agent, which leads to cognitive deficits, synaptic protein decline, tau phosphorylation, oxidative stress, and amyloid plaque accumulation. Another method includes ICV injection of amyloid-β (Aβ) peptides, mimicking AD pathology and inducing cognitive impairment. Additionally, systemic immune challenges using PolyI:C during gestation and adulthood have been shown to predispose mice to AD-like neuropathology, including amyloid precursor protein accumulation, altered tau phosphorylation, and memory impairments. These models provide valuable tools for studying AD pathogenesis and evaluating potential therapeutic interventions.
How stem cell therapy used in Alzheimer?5 answersStem cell therapy is being investigated as a potential treatment for Alzheimer's disease (AD). Different types of stem cells, including embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), mesenchymal stem cells (MSCs), and neural stem cells (NSCs), have been studied for their therapeutic potential in AD. Preclinical studies have shown that stem cell therapy can induce relevant effects in AD, such as improving cognitive performance and promoting neurogenesis. However, there are challenges associated with each type of stem cell, such as controlling differentiation and low survival and homing rates after transplantation. Despite these challenges, stem cell therapy holds promise for AD treatment and could potentially be adapted for other neurodegenerative diseases as well. Future research should focus on studying various types of stem cells, conducting cross-disciplinary research, and improving the timeliness and individualization of stem cell therapies for AD.
What are the new study in tissue engineering in alzheimer disease?5 answersTissue engineering studies in Alzheimer's disease (AD) have focused on developing three-dimensional (3D) culture models to mimic the native microenvironment of the brain. These models utilize induced pluripotent stem cells (iPSCs) derived from AD patients to generate neural tissue. One approach involves using a porous silk-collagen scaffold combined with a collagen hydrogel to support the growth of neurons and glial cells, allowing for the development of complex and functional networks. Another approach involves encapsulating iPSC-derived neural progenitor cells in poly(lactic-co-glycolic acid) (PLGA) microtopographic scaffolds, which accelerates neuronal differentiation and enhances the pathogenic characteristics of familial AD (FAD) mutations. Additionally, a novel organotypic brain slice culture model using transgenic mouse models expressing AD-related genes has been developed, providing a valid and sensitive replacement for in vivo studies. These tissue engineering approaches offer valuable tools for studying AD-related pathomechanisms and testing potential therapeutic interventions.