Protein misfolding and aggregation is observed in many amyloidogenic diseases affecting either the central nervous system or a variety of peripheral tissues. Structural and dynamic characterization of all species along the pathways from monomers to fibrils is challenging by experimental and computational means because they involve intrinsically disordered proteins in most diseases. Yet understanding how amyloid species become toxic is the challenge in developing a treatment for these diseases. Here we review what computer, in vitro, in vivo, and pharmacological experiments tell us about the accumulation and deposition of the oligomers of the (Aβ, tau), α-synuclein, IAPP, and superoxide dismutase 1 proteins, which have been the mainstream concept underlying Alzheimer's disease (AD), Parkinson's disease (PD), type II diabetes (T2D), and amyotrophic lateral sclerosis (ALS) research, respectively, for many years.

Amyloid oligomers: A joint experimental/computational perspective on Alzheimer's disease, Parkinson's disease, type II diabetes, and amyotrophic lateral sclerosis

Since the ferromagnetic (Fe3O4) nanoparticles were firstly reported to exert enzyme-like activity in 2007, extensive research progress in nanozymes has been made with deep investigation of diverse nanozymes and rapid development of related nanotechnologies. As promising alternatives for natural enzymes, nanozymes have broadened the way toward clinical medicine, food safety, environmental monitoring, and chemical production. The past decade has witnessed the rapid development of metal- and metal oxide-based nanozymes owing to their remarkable physicochemical properties in parallel with low cost, high stability, and easy storage. It is widely known that the deep study of catalytic activities and mechanism sheds significant influence on the applications of nanozymes. This review digs into the characteristics and intrinsic properties of metal- and metal oxide-based nanozymes, especially emphasizing their catalytic mechanism and recent applications in biological analysis, relieving inflammation, antibacterial, and cancer therapy. We also conclude the present challenges and provide insights into the future research of nanozymes constituted of metal and metal oxide nanomaterials.

/pdf/a-review-on-metal-and-metal-oxide-based-nanozymes-properties-42jd6wb2mo.pdf

A Review on Metal- and Metal Oxide-Based Nanozymes: Properties, Mechanisms, and Applications

Objective To propose a new hypothesis that GABAergic dysfunction in excitatory and inhibitory (E/I) imbalance drives the pathogenesis of Alzheimer's disease (AD). Background Synaptic dysfunction and E/I imbalance emerge decades before the appearance of cognitive decline in AD patients, which contribute to neurodegeneration. Initially, E/I imbalance was thought to occur first, due to dysfunction of the glutamatergic and cholinergic systems. However, new evidence has demonstrated that the GABAergic system, the counterpart of E/I balance and the major inhibitory neurotransmitter system in the central nervous system, is altered enormously and that this contributes to E/I imbalance and further AD pathogenesis. New hypothesis Alterations to the GABAergic system, induced by multiple AD pathogenic or risk factors, contribute to E/I imbalance and AD pathogenesis. Major challenges for the hypothesis This GABAergic hypothesis accounts for many critical questions and common challenges confronting a new hypothesis of AD pathogenesis. More specifically, it explains why amyloid beta (Aβ), β-secretase (BACE1), apolipoprotein E4 gene (APOE e4), hyperactive glia cells, contributes to AD pathogenesis and why age and sex are the risk factors of AD. GABAergic dysfunction promotes the spread of Aβ pathology throughout the AD brain and associated cognitive impairments, and the induction of dysfunction induced by these varied risk factors shares this common neurobiology leading to E/I imbalance. In turn, some of these factors exacerbate GABAergic dysfunction and E/I imbalance. Moreover, the GABAergic system modulates various brain functions and thus, the GABAergic hypothesis accounts for nonamnestic manifestations. Furthermore, corrections of E/I balance through manipulation of GABAergic functions have shown positive outcomes in preclinical and clinical studies, suggesting the potential of the GABAergic system as a therapeutic target in AD. Linkage to other major theories Dysfunction of the GABAergic system is induced by multiple critical signaling pathways, which include the existing major theories of AD pathogenesis, such as the Aβ and neuroinflammation hypotheses. In a new perspective, this GABAergic hypothesis accounts for the E/I imbalance and related excitotoxicity, which contribute to cognitive decline and AD pathogenesis. Therefore, the GABAergic system could be a key target to restore, at least partially, the E/I balance and cognitive function in AD patients.

GABAergic dysfunction in excitatory and inhibitory (E/I) imbalance drives the pathogenesis of Alzheimer's disease

Infectious diseases caused by bacteria remain a serious and global problem in human health. Herein, the discovery and application of antibiotics, which has attracted much attention in the past years, has cured numerous infectious diseases and made huge contribution in biomedical field. However, the widespread use of the broad-spectrum antibiotics has led to the serious drug resistance for many human bacterial pathogens. Especially, the bacterial drug resistance decreases the therapeutic effect and leads to high mortality. Inspiringly, the introduction of nanomaterials in biomedical field makes it possible to overcome the difficulty in the bacterial drug resistance attributed to their unique antibacterial mechanism. Recently, a variety of metal- and metal oxide-based nanomaterials are fully integrated in antibacterial applications and achieve excellent performances. Among them, cerium and cerium oxide-based nanomaterials have received much attention worldwide. Remarkably, cerium oxide nanoparticles with lower toxicity act as effective antibacterial agents owing to their unique functional mechanism against pathogens through the reversible conversion of oxidation state between Ce(III) and Ce(IV). This article provides an overview of the state-of-the-art design and antibacterial applications of cerium and cerium oxide-based materials. The first part discusses the underlying antibacterial mechanisms for cerium and cerium oxide-based materials currently applied in biomedicine. The second part focuses on various antibacterial related materials and their applications. In addition, the existing problems and future perspectives of the cerium and cerium oxide-based materials make up the third part of this review. This paper could provide the possible mechanisms for antibacterial activities, various designs of cerium and cerium oxide-based materials and related antibacterial properties.

/pdf/cerium-and-its-oxidant-based-nanomaterials-for-antibacterial-crye4w3rlb.pdf

Cerium and its oxidant based nanomaterials for antibacterial applications: A state-of-the- art review

Aging causes many changes in the human body, and is a high risk for various diseases. Dementia, a common age-related disease, is a clinical disorder triggered by neurodegeneration. Brain damage caused by neuronal death leads to cognitive decline, memory loss, learning inabilities and mood changes. Numerous disease conditions may cause dementia; however, the most common one is Alzheimer’s disease (AD), a futile and yet untreatable illness. Adult neurogenesis carries the potential of brain self-repair by an endogenous formation of newly-born neurons in the adult brain; however it also declines with age. Strategies to improve the symptoms of aging and age-related diseases have included different means to stimulate neurogenesis, both pharmacologically and naturally. Finally, the regulatory mechanisms of stem cells neurogenesis or a functional integration of newborn neurons have been explored to provide the basis for grafted stem cell therapy. This review aims to provide an overview of AD pathology of different neural and glial cell types and summarizes current strategies of experimental stem cell treatments and their putative future use in clinical settings.

Neurodegeneration and Neuro-Regeneration-Alzheimer's Disease and Stem Cell Therapy

We propose a new blind spread spectrum image watermarking approach in Contourlet domain for securing face recognition systems. This will prevent the replacement of genuine face images by imposter ones. We have calculated the performance of a PCA-based face recognition system with and without watermarking under several attacks including addition of noise, filtering, JPEG lossy compression, and rotation. The results of experimentations showed that addition of a watermarking part to the system have no important degradation effect on the face recognition performance.

Image Watermarking in Face Recognition Systems Based on Contourlet Transform

In this paper we survey the inventory problem for item's which delay occurred for supply them. In this situation the shortage of inventory happen and order which encounter shortage, will increase and make backorders and impose new costs on inventory system and impact on optimal quantity of order in EOQ model. Since in practice and in real situations we don't have accurate value for much data of model, we determine the optimal order quantity in fuzzy sense. For this objective first we consider an EOQ model with fuzzy costs and then we consider EOQ model with fuzzy backorder and for deffuzify of these two fuzzy models we employ signed distance, a defuzzification method for fuzzy number. At the end of this paper for imply the application of proposed model we mention a numerical example and furthermore we compare the result of fuzzy case with those of crisp case for one item.

Determine the Optimal Order Quantity in Multi-items&s EOQ Model with Backorder


 Spinal cord injury (SCI) can lead to neurological impairment with significant functional and cognitive deficits. It is obvious that SCI causes focal neurodegeneration that gradually expands to the other cord areas. On the other hand, it is clear that traumatic brain injuries result in tau protein pathology and profound neurodegeneration. Tau is a microtubule-associated protein, which is highly expressed in neurons, and its abnormalities result in neuronal cell death. Moreover, it is clear that tau pathology spreads in various brain areas upon trauma. Therefore, we herein examined tau pathology in the spinal cord as well as brain samples at various time-points in severe SCI mouse models. We examined the effects of severe SCI on locomotor function, spatial memory, and anxiety/risk-taking behavior. We found a gradual increased tau pathology in the spinal cord as well as brain areas; confirmed by immunostaining and immunoblotting. Moreover, we studied the brain samples with electron microscopy and observed disrupted mitochondria and microtubule structure upon SCI. SCI caused motor dysfunction, memory impairment, and abnormal risk-taking behavior. Importantly, pathogenic cis P-tau elimination with systemic administration of respective monoclonal antibody restored SCI-related pathological and functional consequences. Thus, our finding suggests that SCI results in profound tauopathy, which spreads to brain areas, reflecting brain dysfunction. Moreover, tau immunotherapy with anti-cis P-tau antibody could suppress the pathogenic outcomes in the SCI mouse models, which would have profound clinical implications in the SCI patients.

/pdf/spinal-cord-injury-causes-prominent-tau-pathology-associated-46dl3gcxtb.pdf

Spinal Cord Injury Causes Prominent Tau Pathology Associated with Brain Post-Injury Sequela

Bipolar disorder is a complex neuropsychiatric disorder, characterized by intermittent episodes of mania and depression. Recent studies have indicated argyrophilic grains, composed of hyperphosphorylated tau, are observable in postmortem brains of bipolar patients. It remains uncertain how tau hyperphosphorylation results in neurodegeneration upon the disease. Recent studies have demonstrated that phosphorylated tau at Thr231 exists in two distinct cis and trans conformations, in which cis pT231-tau is highly neurotoxic and acts as an early driver of tauopathy in several neurodegenerative diseases. We herein employed an in vitro model, which resembles some aspects of bipolar disorder, to study the cis p-tau mediatory role. We established GSK3β overexpressing SH-SY5Y cells and examined cell viability, cis p-tau formation, and lithium effects by immunofluorescence and flow cytometry. We found an increase in cis p-tau levels as well as viability decrease in the cell model. Furthermore, we discovered that lithium treatment inhibits cis p-tau formation, resulting in diminished cell death. We also examined BD and healthy human brain samples and detected cis p-tau in the patients' brains. Our results show that tauopathy, observed in bipolar disorder, is being mediated through cis p-tau and that a conformer could be the cause of neurodegeneration upon the disease. Our findings would suggest novel therapeutic target to fight the devastating disorder.

cis pT231-Tau Drives Neurodegeneration in Bipolar Disorder

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Ehsan Ehsani

Author Tools

Chat about Author

Papers

Image Watermarking in Face Recognition Systems Based on Contourlet Transform

Determine the Optimal Order Quantity in Multi-items&s EOQ Model with Backorder

Spinal Cord Injury Causes Prominent Tau Pathology Associated with Brain Post-Injury Sequela

cis pT231-Tau Drives Neurodegeneration in Bipolar Disorder