https://espace.library.uq.edu.au/view/UQ:d04f513/UQd04f513_OA.pdf

Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation.

Alzheimer’s disease (AD) is a neurodegenerative disease associated with human aging. Ten percent of individuals over 65 years have AD and its prevalence continues to rise with increasing age. There are currently no effective disease modifying treatments for AD, resulting in increasingly large socioeconomic and personal costs. Increasing age is associated with an increase in low-grade chronic inflammation (inflammaging) that may contribute to the neurodegenerative process in AD. Although the exact mechanisms remain unclear, aberrant elevation of reactive oxygen and nitrogen species (RONS) levels from several endogenous and exogenous processes in the brain may not only affect cell signaling, but also trigger cellular senescence, inflammation, and pyroptosis. Moreover, a compromised immune privilege of the brain that allows the infiltration of peripheral immune cells and infectious agents may play a role. Additionally, meta-inflammation as well as gut microbiota dysbiosis may drive the neuroinflammatory process. Considering that inflammatory/immune pathways are dysregulated in parallel with cognitive dysfunction in AD, elucidating the relationship between the central nervous system and the immune system may facilitate the development of a safe and effective therapy for AD. We discuss some current ideas on processes in inflammaging that appear to drive the neurodegenerative process in AD and summarize details on a few immunomodulatory strategies being developed to selectively target the detrimental aspects of neuroinflammation without affecting defense mechanisms against pathogens and tissue damage.

Neuroinflammation in Alzheimer's Disease.

Alzheimer’s disease (AD) is a neurodegenerative disorder molecularly characterized by the formation of amyloid β (Aβ) plaques and type 2 microtubule-associated protein (Tau) abnormalities. Multiple studies have shown that many of the brain’s immunological cells, specifically microglia and astrocytes, are involved in AD pathogenesis. Cells of the innate immune system play an essential role in eliminating pathogens but also regulate brain homeostasis and AD. When activated, innate immune cells can cause programmed cell death through multiple pathways, including pyroptosis, apoptosis, necroptosis, and PANoptosis. The cell death often results in the release of proinflammatory cytokines that propagate the innate immune response and can eliminate Aβ plaques and aggregated Tau proteins. However, chronic neuroinflammation, which can result from cell death, has been linked to neurodegenerative diseases and can worsen AD. Therefore, the innate immune response must be tightly balanced to appropriately clear these AD-related structural abnormalities without inducing chronic neuroinflammation. In this review, we discuss neuroinflammation, innate immune responses, inflammatory cell death pathways, and cytokine secretion as they relate to AD. Therapeutic strategies targeting these innate immune cell death mechanisms will be critical to consider for future preventive or palliative treatments for AD.

/pdf/innate-immune-cell-death-in-neuroinflammation-and-alzheimers-13xiijmi.pdf

Innate Immune Cell Death in Neuroinflammation and Alzheimer’s Disease

Epilepsy is a disease characterized by recurrent, episodic, and transient central nervous system (CNS) dysfunction resulting from an excessive synchronous discharge of brain neurons. It is characterized by diverse etiology, complex pathogenesis, and difficult treatment. In addition, most epileptic patients exhibit social cognitive impairment and psychological impairment. Iron is an essential trace element for human growth and development and is also involved in a variety of redox reactions in organisms. However, abnormal iron metabolism is associated with several neurological disorders, including hemorrhagic post-stroke epilepsy and post-traumatic epilepsy (PTE). Moreover, ferroptosis is also considered a new form of regulation of cell death, which is attributed to severe lipid peroxidation caused by the production of reactive oxygen species (ROS) and iron overload found in various neurological diseases, including epilepsy. Therefore, this review summarizes the study on iron metabolism and ferroptosis in epilepsy, in order to elucidate the correlation between iron and epilepsy. It also provides a novel method for the treatment, prevention, and research of epilepsy, to control epileptic seizures and reduce nerve injury after the epileptic seizure.

/pdf/iron-metabolism-and-ferroptosis-in-epilepsy-3lm9t5mz8b.pdf

Iron Metabolism and Ferroptosis in Epilepsy.

In recent years, many promising nanotechnological approaches to biomedical research have been developed in order to increase implementation of regenerative medicine and tissue engineering in clinical practice. In the meantime, the use of nanomaterials for the regeneration of diseased or injured tissues is considered advantageous in most areas of medicine. In particular, for the treatment of cardiovascular, osteochondral and neurological defects, but also for the recovery of functions of other organs such as kidney, liver, pancreas, bladder, urethra and for wound healing, nanomaterials are increasingly being developed that serve as scaffolds, mimic the extracellular matrix and promote adhesion or differentiation of cells. This review focuses on the latest developments in regenerative medicine, in which iron oxide nanoparticles (IONPs) play a crucial role for tissue engineering and cell therapy. IONPs are not only enabling the use of non-invasive observation methods to monitor the therapy, but can also accelerate and enhance regeneration, either thanks to their inherent magnetic properties or by functionalization with bioactive or therapeutic compounds, such as drugs, enzymes and growth factors. In addition, the presence of magnetic fields can direct IONP-labeled cells specifically to the site of action or induce cell differentiation into a specific cell type through mechanotransduction.

/pdf/iron-oxide-nanoparticles-in-regenerative-medicine-and-tissue-2xxxoyc4k4.pdf

Iron Oxide Nanoparticles in Regenerative Medicine and Tissue Engineering.

OBJECTIVEIntraventricular hemorrhage (IVH) is found in approximately 40% of intracerebral hemorrhages and is associated with increased mortality and poor functional outcome. Cognitive impairment is one of the complications and occurs due to various pathological changes. Amyloid beta (Aβ) accumulation and neuroinflammation, and the Alzheimer disease–like pathology, may contribute to cognitive impairment. Iron, the degradation product of hemoglobin, correlates with Aβ. In this study, the authors investigated the correlation between Aβ accumulation with enhanced neuroinflammation and cognitive impairment in a rat model of IVH.METHODSNine male Sprague-Dawley rats underwent an intraventricular injection of autologous blood. Another 9 rats served as controls. Cognitive function was assessed by the Morris water maze and T-maze rewarded alternation tests. Biomarkers of Aβ accumulation, neuroinflammation, and c-Jun N-terminal kinase (JNK) activation were examined.RESULTSCognitive function was impaired in the autol...

The correlation between accumulation of amyloid beta with enhanced neuroinflammation and cognitive impairment after intraventricular hemorrhage

Effectiveness of deferoxamine on ferric chloride-induced epilepsy in rats

Stroke is one of the top three fatal diseases in human history. Inflammatory injury of the artery endo-membrane system is widely accepted as the major starting mechanism for the formation and enlargement of atherosclerosis plaque, which can be diagnosed by B-ultrasound or carotid angiography. However, clinical data reveal that there are asymptomatic patients that are not diagnosed until the stenosis degree is over 70%. Superparamagnetic iron oxide (SPIO), a promising candidate for a next generation contrast agent in medical imaging, has been used in the imaging of carotid artery plaques, but it still faces the challenge of targeted enrichment. Herein, we introduce a mature magnetic nanoparticle contrast agent and a promising method for diagnosing carotid artery inflammatory plaques with a Magnetic Resonance Imaging (MRI) technique. The superparamagnetic nanoparticles (SNPs) were synthesized by directly coating hydrophilic and high-magnetism Fe3O4 nanoparticles with an organosilica layer, which was followed by modification with polyethylene glycol. It was verified that the resultant nanocomposite possesses a higher structural stability, excellent dispersivity, separability, as well as biosafety. More importantly, the strong magnetism was preserved, making it possible to attract the SNPs with an external magnetic field and achieve a target concentration within the lesion. Moreover, an in vitro magnetic collar, designed to produce a stable magnetic field around the superficial common carotid arteries was introduced. The SNPs particles in the blood flow were slowed down by the collar, their motion direction was changed, and they were captured by the inflammatory cells in the plaque. The effectiveness and feasibility of the particles were evaluated via testing the MRI performance on histological levels with a rat carotid plaque model. The SNPs that were concentrated and accumulated in the plaque were verified to present an evident, negative enhancement in the Proton Density-T2 (PD-T2) sequence images. Therefore, it was demonstrated that the superparamagnetic nanoparticles have great potential as an MRI contrast agent to detect early stage carotid artery inflammatory plaques with an external magnetic collar.

Imaging of carotid artery inflammatory plaques with superparamagnetic nanoparticles and an external magnet collar

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The correlation between accumulation of amyloid beta with enhanced neuroinflammation and cognitive impairment after intraventricular hemorrhage

Effectiveness of deferoxamine on ferric chloride-induced epilepsy in rats

Imaging of carotid artery inflammatory plaques with superparamagnetic nanoparticles and an external magnet collar