Relevant bibliographies by topics / Cadmium, blood-brain barrier, neurodegenerative diseases

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cadmium, blood-brain barrier, neurodegenerative diseases'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Cadmium, blood-brain barrier, neurodegenerative diseases"

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Branca, Jacopo Junio Valerio, Mario Maresca, Gabriele Morucci, Tommaso Mello, Matteo Becatti, Luigia Pazzagli, Ilaria Colzi, et al. "Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier." International Journal of Molecular Sciences 20, no. 23 (November 29, 2019): 6010. http://dx.doi.org/10.3390/ijms20236010.

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Cadmium (Cd) is a highly toxic environmental pollutant released from the smelting and refining of metals and cigarette smoking. Oral exposure to cadmium may result in adverse effects on a number of tissues, including the central nervous system (CNS). In fact, its toxicity has been related to neurological disorders, as well as neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases. Under normal conditions, Cd barely reaches the brain in adults because of the presence of the blood–brain barrier (BBB); however, it has been demonstrated that Cd-dependent BBB alteration contributes to pathogenesis of neurodegeneration. However, the mechanism underlying Cd-dependent BBB alteration remain obscure. Here, we investigated the signaling pathway of Cd-induced tight junction (TJ), F-actin, and vimentin protein disassembly in a rat brain endothelial cell line (RBE4). RBE4 cells treated with 10 μM cadmium chloride (CdCl2) showed a dose- and time-dependent significant increase in reactive oxygen species (ROS) production. This phenomenon was coincident with the alteration of the TJ zonula occludens-1 (ZO-1), F-actin, and vimentin proteins. The Cd-dependent ROS increase elicited the upregulation of GRP78 expression levels, a chaperone involved in endoplasmic reticulum (ER) stress that induces caspase-3 activation. Further signal profiling by the pannexin-1 (PANX1) specific inhibitor 10Panx revealed a PANX1-independent increase in ATP spillage in Cd-treated endothelial cells. Our results point out that a ROS-dependent ER stress-mediated signaling pathway involving caspase-3 activation and ATP release is behind the BBB morphological alterations induced by Cd.
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Bressler, Joseph P., Luisa Olivi, Jae Hoon Cheong, Yongbae Kim, Alex Maerten, and Desmond Bannon. "Metal transporters in intestine and brain: their involvement in metal-associated neurotoxicities." Human & Experimental Toxicology 26, no. 3 (March 2007): 221–29. http://dx.doi.org/10.1177/0960327107070573.

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The transport of essential metals and other nutrients across tightmembrane barriers such as the gastrointestinal tract and blood-brain barrier is mediated by specific transport mechanisms. Specific transporters take up metals at the apical surface and export them at the basolateral surface, and are involved in their intracellular distribution. Transporters for each of the major essential metals, calcium, iron and zinc, have been identified. These transporters also mediate the transport of non-essential metals across tight membrane barriers. For example, the intestinal iron transporter divalent metal transporter 1 mediates the uptake of lead and cadmium. The levels of essential metals are strictly regulated by transporters. When dietary levels of essential metals are low, levels of the corresponding transporters increase in the intestine, after which there is a greater potential for increased transport of toxic metals. In the brain, the strict regulation of metals prevents injury that potentially would result from oxidative damage induced by the essential metals iron, copper and zinc. Indeed, the oxidative damage found in neurodegenerative diseases is likely to be due to higher levels of these metals. Involvement of intracellular transporters for copper and zinc has been shown in animal models of Alzheimer's disease, raising the possibility that higher levels of iron, zinc and copper might be due to a disruption in the activity of transporters. Accordingly, exposure to toxicants that affect the activity of transporters potentially could contribute to the aetiology/progression of neurodegenerative diseases.
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Kakaroubas, Nicholas, Samuel Brennan, Matthew Keon, and Nitin K. Saksena. "Pathomechanisms of Blood-Brain Barrier Disruption in ALS." Neuroscience Journal 2019 (July 10, 2019): 1–16. http://dx.doi.org/10.1155/2019/2537698.

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The blood-brain barrier (BBB) and the blood-spinal cord barrier (BSCB) are responsible for controlling the microenvironment within neural tissues in humans. These barriers are fundamental to all neurological processes as they provide the extreme nutritional demands of neural tissue, remove wastes, and maintain immune privileged status. Being a semipermeable membrane, both the BBB and BSCB allow the diffusion of certain molecules, whilst restricting others. In amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases, these barriers become hyperpermeable, allowing a wider variety of molecules to pass through leading to more severe and more rapidly progressing disease. The intention of this review is to discuss evidence that BBB hyperpermeability is potentially a disease driving feature in ALS and other neurodegenerative diseases. The various biochemical, physiological, and genomic factors that can influence BBB permeability in ALS and other neurodegenerative diseases are also discussed, in addition to novel therapeutic strategies centred upon the BBB.
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Weber, Callie M., and Alisa Morss Clyne. "Sex differences in the blood–brain barrier and neurodegenerative diseases." APL Bioengineering 5, no. 1 (March 1, 2021): 011509. http://dx.doi.org/10.1063/5.0035610.

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Karamanos, Yannis, Fabien Gosselet, Marie-Pierre Dehouck, and Roméo Cecchelli. "Blood–Brain Barrier Proteomics: Towards the Understanding of Neurodegenerative Diseases." Archives of Medical Research 45, no. 8 (November 2014): 730–37. http://dx.doi.org/10.1016/j.arcmed.2014.11.008.

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Wu, Ying-Chieh, Tuuli-Maria Sonninen, Sanni Peltonen, Jari Koistinaho, and Šárka Lehtonen. "Blood–Brain Barrier and Neurodegenerative Diseases—Modeling with iPSC-Derived Brain Cells." International Journal of Molecular Sciences 22, no. 14 (July 19, 2021): 7710. http://dx.doi.org/10.3390/ijms22147710.

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The blood–brain barrier (BBB) regulates the delivery of oxygen and important nutrients to the brain through active and passive transport and prevents neurotoxins from entering the brain. It also has a clearance function and removes carbon dioxide and toxic metabolites from the central nervous system (CNS). Several drugs are unable to cross the BBB and enter the CNS, adding complexity to drug screens targeting brain disorders. A well-functioning BBB is essential for maintaining healthy brain tissue, and a malfunction of the BBB, linked to its permeability, results in toxins and immune cells entering the CNS. This impairment is associated with a variety of neurological diseases, including Alzheimer’s disease and Parkinson’s disease. Here, we summarize current knowledge about the BBB in neurodegenerative diseases. Furthermore, we focus on recent progress of using human-induced pluripotent stem cell (iPSC)-derived models to study the BBB. We review the potential of novel stem cell-based platforms in modeling the BBB and address advances and key challenges of using stem cell technology in modeling the human BBB. Finally, we highlight future directions in this area.
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Sharma, Chanchal, Hanwoong Woo, and Sang Ryong Kim. "Addressing Blood–Brain Barrier Impairment in Alzheimer’s Disease." Biomedicines 10, no. 4 (March 22, 2022): 742. http://dx.doi.org/10.3390/biomedicines10040742.

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The blood–brain barrier (BBB) plays a vital role in maintaining the specialized microenvironment of the brain tissue. It facilitates communication while separating the peripheral circulation system from the brain parenchyma. However, normal aging and neurodegenerative diseases can alter and damage the physiological properties of the BBB. In this review, we first briefly present the essential pathways maintaining and regulating BBB integrity, and further review the mechanisms of BBB breakdown associated with normal aging and peripheral inflammation-causing neurodegeneration and cognitive impairments. We also discuss how BBB disruption can cause or contribute to Alzheimer’s disease (AD), the most common form of dementia and a devastating neurological disorder. Next, we document overlaps between AD and vascular dementia (VaD) and briefly sum up the techniques for identifying biomarkers linked to BBB deterioration. Finally, we conclude that BBB breakdown could be used as a biomarker to help diagnose cognitive impairment associated with normal aging and neurodegenerative diseases such as AD.
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Cui, Weitong, Wei Fu, Yunfeng Lin, and Tianxu Zhang. "Application of Nanomaterials in Neurodegenerative Diseases." Current Stem Cell Research & Therapy 16, no. 1 (December 1, 2021): 83–94. http://dx.doi.org/10.2174/1574888x15666200326093410.

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Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease are very harmful brain lesions. Due to the difficulty in obtaining therapeutic drugs, the best treatment for neurodegenerative diseases is often not available. In addition, the bloodbrain barrier can effectively prevent the transfer of cells, particles and macromolecules (such as drugs) in the brain, resulting in the failure of the traditional drug delivery system to provide adequate cellular structure repair and connection modes, which are crucial for the functional recovery of neurodegenerative diseases. Nanomaterials are designed to carry drugs across the blood-brain barrier for targets. Nanotechnology uses engineering materials or equipment to interact with biological systems at the molecular level to induce physiological responses through stimulation, response and target site interactions, while minimizing the side effects, thus revolutionizing the treatment and diagnosis of neurodegenerative diseases. Some magnetic nanomaterials play a role as imaging agents or nanoprobes for Magnetic Resonance Imaging to assist in the diagnosis of neurodegenerative diseases. Although the current research on nanomaterials is not as useful as expected in clinical applications, it achieves a major breakthrough and guides the future development direction of nanotechnology in the application of neurodegenerative diseases. This review briefly discusses the application and advantages of nanomaterials in neurodegenerative diseases. Data for this review were identified by searches of PubMed, and references from relevant articles published in English between 2015 and 2019 using the search terms “nanomaterials”, “neurodegenerative diseases” and “blood-brain barrier”.
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Silva Adaya, Daniela, Lucinda Aguirre-Cruz, Jorge Guevara, and Emma Ortiz-Islas. "Nanobiomaterials’ applications in neurodegenerative diseases." Journal of Biomaterials Applications 31, no. 7 (November 11, 2016): 953–84. http://dx.doi.org/10.1177/0885328216659032.

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The blood–brain barrier is the interface between the blood and brain, impeding the passage of most circulating cells and molecules, protecting the latter from foreign substances, and maintaining central nervous system homeostasis. However, its restrictive nature constitutes an obstacle, preventing therapeutic drugs from entering the brain. Usually, a large systemic dose is required to achieve pharmacological therapeutic levels in the brain, leading to adverse effects in the body. As a consequence, various strategies are being developed to enhance the amount and concentration of therapeutic compounds in the brain. One such tool is nanotechnology, in which nanostructures that are 1–100 nm are designed to deliver drugs to the brain. In this review, we examine many nanotechnology-based approaches to the treatment of neurodegenerative diseases. The review begins with a brief history of nanotechnology, followed by a discussion of its definition, the properties of most reported nanomaterials, their biocompatibility, the mechanisms of cell–material interactions, and the current status of nanotechnology in treating Alzheimer’s, Parkinson’s diseases, and amyotrophic lateral sclerosis. Of all strategies to deliver drug to the brain that are used in nanotechnology, drug release systems are the most frequently reported.
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Fang, Yao-Ching, Yi-Chen Hsieh, Chaur-Jong Hu, and Yong-Kwang Tu. "Endothelial Dysfunction in Neurodegenerative Diseases." International Journal of Molecular Sciences 24, no. 3 (February 2, 2023): 2909. http://dx.doi.org/10.3390/ijms24032909.

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The cerebral vascular system stringently regulates cerebral blood flow (CBF). The components of the blood–brain barrier (BBB) protect the brain from pathogenic infections and harmful substances, efflux waste, and exchange substances; however, diseases develop in cases of blood vessel injuries and BBB dysregulation. Vascular pathology is concurrent with the mechanisms underlying aging, Alzheimer’s disease (AD), and vascular dementia (VaD), which suggests its involvement in these mechanisms. Therefore, in the present study, we reviewed the role of vascular dysfunction in aging and neurodegenerative diseases, particularly AD and VaD. During the development of the aforementioned diseases, changes occur in the cerebral blood vessel morphology and local cells, which, in turn, alter CBF, fluid dynamics, and vascular integrity. Chronic vascular inflammation and blood vessel dysregulation further exacerbate vascular dysfunction. Multitudinous pathogenic processes affect the cerebrovascular system, whose dysfunction causes cognitive impairment. Knowledge regarding the pathophysiology of vascular dysfunction in neurodegenerative diseases and the underlying molecular mechanisms may lead to the discovery of clinically relevant vascular biomarkers, which may facilitate vascular imaging for disease prevention and treatment.
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Dissertations / Theses on the topic "Cadmium, blood-brain barrier, neurodegenerative diseases"

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Leoni, Valerio. "On the possible use of oxysterols for the diagnosis and evaluation of patients with neurological and neurodegenerative diseases /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-255-1/.

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Carrino, Donatello. "Effetti biologici dell'esposizione cronica al cadmio sulla barriera emato-encefalica." Doctoral thesis, 2022. http://hdl.handle.net/2158/1263776.

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Over the years, anthropogenic factors have led to cadmium (Cd) accumulation in the environment causing various health problems. Due to its highly soluble nature compared to other metals, Cd is easily absorbed by plants, giving rise to bioaccumulation phenomena. Thus, diet is the primary source of Cd exposure in humans. Other sources include smoking, occupational exposure and indoor spaces, particularly exposed to the metal. Once inside the bloodstream, Cd is capable of damaging the blood-brain barrier (BBB), a specialized system that shields the central nervous system (CNS) from toxic substances in the blood. This impairment allows a greater amount of the neurotoxic to enter the CNS leading to neurodegeneration. In fact, chronic exposure to Cd has been linked to numerous neurodegenerative disorders in adulthood, including Alzheimer’s and Parkinson’s disease. Although in vivo studies have established a Cd-dependent BBB dysfunction, the molecular mechanisms underlying the increased permeability of the barrier have not yet been fully elucidated. In this work, possible molecular pathways involved in the disassembly of tight junctions in a rat brain endothelium (RBE4) cell line have been outlined, as an in vitro model for the study of the BBB. This phenomenon coincided with the upregulation of GRP78 expression levels, a chaperone involved in the endoplasmic reticulum stress, and the activation of caspase-3. The cellular response to oxidative stress was also evaluated by the subcellular localization of Nrf2 and the consequent expression of SOD1, as part of a defense mechanism to counteract Cd-induced damage. On the other hand, the micronutrient Zinc (Zn), one of the most important microelements necessary for normal body functioning, was able to mitigate Cd harmful effects, partially preventing ZO-1 dislocation and altered cytoskeleton rearrangements. Based on the experimental data, Zn is able to interfere with the toxic action exerted by Cd, suggesting its diet integration as an effective strategy to hinder cellular oxidative stress, helping to maintain the barrier integrity. Cd neurotoxic effects on RBE4 cells were also evaluated in co-culture to determine whether these effects could be modulated in the presence of the other cell types that form the neurovascular unit, such as DI TNC1 astrocytes and RBVP pericytes. The results clearly showed that Cd influences mitochondrial activity and cell morphology even in co-culture conditions, but that the cytotoxic effects were dampened in the presence of astrocytes, but not pericytes. In addition, the support function of astrocytes highlighted their leading role in strengthening the tight junction structural complexes by the expression of adhesion molecules such as claudin-5.
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Ribeiro, Adriana Marques. "Relatório de Estágio em Farmácia Comunitária e Monografia intitulada “The Role of the Blood-Brain Barrier and the Application of Nanomedicines in Neurodegenerative Diseases”." Master's thesis, 2019. http://hdl.handle.net/10316/88332.

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Relatório de Estágio do Mestrado Integrado em Ciências Farmacêuticas apresentado à Faculdade de Farmácia
A Faculdade de Farmácia da Universidade de Coimbra, através do Mestrado Integrado em Ciências Farmacêuticas, tem como objetivo preparar os alunos para o desenvolvimento de atividades relacionadas com o medicamento e com a Saúde. Uma das áreas fundamentais, e também das mais antigas, com origem nos antigos boticários e nas suas boticas, é a Farmácia de Oficina ou, como atualmente é conhecida, a Farmácia Comunitária. “Comunitária” advém de comunidade, na sua capacidade de destinatária da ação farmacêutica, englobada no objetivo da promoção do bem-estar e da saúde e não apenas da ausência da doença. O relatório de estágio, elaborado sob a forma de análise SWOT visa expor a experiência do estágio em Farmácia Comunitária, realizado na Sucursal de Coimbra do Laboratório Militar de Produtos Químicos e Farmacêuticas no decorrer do último ano do mestrado. As Doenças Neurodegenerativas são um conjunto de doenças que afetam os neurónios do Sistema Nervoso Central. Exemplos destas doenças são a Doença de Parkinson e a Doença de Alzheimer. Estas patologias tomam conta da vida dos pacientes que as detêm e são obstáculo à existência de uma vida em pleno devido à degeneração progressiva do sistema nervoso e consequentes sintomas. A descoberta de terapêuticas realmente eficazes pode vir a revolucionar o dia-a-dia dos doentes e das pessoas que os rodeiam. Uma aproximação terapêutica possível é a Nanomedicina, que recorre a sistemas de escala nanométrica. Estes podem contornar obstáculos fisiológicos como a Barreira Hematoencefálica, uma barreira que tem como função proteger, mas também que se torna um desafio à passagem de terapêuticas convencionais.A presente monografia pretende abordar os desafios impostos pela Barreira Hematoencefálica como barreira física à passagem de terapêuticas convencionais e quais os nanosistemas atualmente descritos que podem vir a ser promessas na terapêutica das Doenças Neurodegenerativas.
The Faculty of Pharmacy of the University of Coimbra, through the Integrated Master in Pharmaceutical Sciences, has the aim to prepare the students for the development of activities related to Health and Medicines.One of the fundamental areas and one of the oldest ones, dated back to the old apothecaries, is Community Pharmacy. This area relates us to Community, the recipient of the pharmacist’s role in providing health care, trough the promotion of health and well-being and not only by the absence of disease. The internship report, based on SWOT analysis, gives an overlook about the experience of the Internship in Community Pharmacy, carried out in the Military Laboratory of Chemical and Pharmaceutical Products, in Coimbra’s branch, over the course of the last academic year of the Integrated Master. Neurodegenerative Diseases are a group of conditions that affect neurons of the Central Nervous System. Examples of these diseases are Parkinson's Disease and Alzheimer's Disease. These pathologies take care of the life of the patients and do not allow them to have a full life due to the progressive degeneration of the nervous system and consequent symptoms. The discovery of truly effective therapies can revolutionize the day-to-day lives of patients and those around them.One possible therapeutic approach is Nanomedicine, which uses nanoscale systems that can circumvent physiological obstacles such as the Blood-Brain Barrier, a barrier which function is to protect but also becomes a challenge to the passage of conventional therapies.The present monograph aims to address the challenges posed by the Blood-Brain Barrier as a physical obstacle to the passage of conventional therapies and the currently described nanosystems can be promising in the therapy of Neurodegenerative Diseases.
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Books on the topic "Cadmium, blood-brain barrier, neurodegenerative diseases"

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Di, Liegro Italia, and Savettieri Giovanni, eds. Molecular bases of neurodegeneration, 2005. Kerala, India: Research Signpost, 2005.

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Gupta, Anil. Blood-Brain Barrier in Neurodegenerative Diseases: New Perspectives in Neuropathology. Elsevier Science & Technology Books, 2024.

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Book chapters on the topic "Cadmium, blood-brain barrier, neurodegenerative diseases"

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Youdim, M. B. H., K. L. Leenders, and D. Ben-Shachar. "Brain Iron Uptake and Transport in Animal Model of Iron Deficiency, Tardive Dyskinesia and Neurodegenerative Diseases." In Blood—Brain Barrier, 147–56. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0579-2_12.

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Peschanski, Marc. "Prospects for Neuroprotective Gene Therapy for Neurodegenerative Diseases." In Biology and Physiology of the Blood-Brain Barrier, 9–10. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_2.

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Ribatti, Domenico. "Mast Cells in Blood-Brain Barrier Alterations and Neurodegenerative Diseases." In The Mast Cell, 67–74. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24190-2_8.

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Maher, Barbara A. "Airborne Magnetite- and Iron-Rich Pollution Nanoparticles: Potential Neurotoxicants and Environmental Risk Factors for Neurodegenerative Disease, Including Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210006.

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Fewer than 5% of Alzheimer’s disease (AD) cases are demonstrably directly inherited, indicating that environmental factors may be important in initiating and/or promoting the disease. Excess iron is toxic to cells; iron overload in the AD brain may aggressively accelerate AD. Magnetite nanoparticles, capable of catalyzing formation of reactive oxygen species, occur in AD plaques and tangles; they are thought to form in situ, from pathological iron dysfunction. A recent study has identified in frontal cortex samples the abundant presence of magnetite nanoparticles consistent with high-temperature formation; identifying therefore their external, not internal source. These magnetite particles range from ∼10 to 150 nm in size, and are often associated with other, non-endogenous metals (including platinum, cadmium, cerium). Some display rounded crystal morphologies and fused surface textures, reflecting cooling and crystallization from an initially heated, iron-bearing source material. Precisely-matching magnetite ‘nanospheres’ occur abundantly in roadside air pollution, arising from vehicle combustion and, especially, frictional brake-wear. Airborne magnetite pollution particles <∼200 nm in size can access the brain directly via the olfactory and/or trigeminal nerves, bypassing the blood-brain barrier. Given their toxicity, abundance in roadside air, and nanoscale dimensions, traffic-derived magnetite pollution nanoparticles may constitute a chronic and pernicious neurotoxicant, and hence an environmental risk factor for AD, for large population numbers globally. Olfactory nerve damage displays strong association with AD development. Reported links between AD and occupational magnetic fields (e.g., affecting welders, machinists) may instead reflect inhalation exposure to airborne magnetic nanoparticles.
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Krishnan, Anuradha, Hao Wu, and Venkat Venkataraman. "Astrocytic S100B, Blood-Brain Barrier and Neurodegenerative Diseases." In Glia in Health and Disease. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92146.

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Braun, Molly, and Jeffrey J. Iliff. "The impact of neurovascular, blood-brain barrier, and glymphatic dysfunction in neurodegenerative and metabolic diseases." In International Review of Neurobiology, 413–36. Elsevier, 2020. http://dx.doi.org/10.1016/bs.irn.2020.02.006.

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Konofagou, Elisa E. "Blood–Brain Barrier Opening and Drug Delivery Using Focused Ultrasound and Microbubbles." In Neurobiology of Mental Illness, edited by Karl Deisseroth, 148–59. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0011.

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Current treatments of neurological and neurodegenerative diseases are limited due to the lack of a truly non-invasive, transient, and regionally selective brain drug delivery method. The brain is particularly difficult to deliver drugs to because of the blood-brain barrier (BBB). The impermeability of the BBB is due to the tight junctions connecting adjacent endothelial cells and highly regulatory transport systems of the endothelial cell membranes. The main function of the BBB is ion and volume regulation to ensure conditions necessary for proper synaptic and axonal signaling. However, the same permeability properties that keep the brain healthy also constitute the cause of the tremendous obstacles posed in its pharmacological treatment. The BBB prevents most neurologically active drugs from entering the brain and, as a result, has been isolated as the rate-limiting factor in brain drug delivery. Until a solution to the trans-BBB delivery problem is found, treatments of neurological diseases will remain impeded. Over the past decade, methods that combine Focused Ultrasound (FUS) and microbubbles have been shown to offer the unique capability of noninvasively, locally and transiently opening the BBB so as to treat central nervous system (CNS) diseases. Four of the main challenges that lie ahead are to: 1) assess its safety profile, 2) unveil the mechanism by which the BBB opens and closes, 3) control and predict the opened BBB properties and duration of the opening and 4) assess its premise in brain drug delivery. All these challenges will be discussed, findings in both small (mice) and large (non-human primates) animals will be shown and finally the case for this technique for clinical applications will be made.
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Adams, Jr., Ph.D., James D. "DNA, Nuclear Cell Signaling and Neurodegeneration." In Extracellular and Intracellular Signaling, 175–87. The Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/bk9781849733434-00175.

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During aging, it is normal for neurodegeneration to occur, sometimes leading to Alzheimer's disease, Parkinson's disease and other conditions. Stroke can cause massive neurodegeneration. There is controversy concerning the causes of these conditions. Lifestyle will be examined as a possible cause of many neurodegenerative conditions in this chapter. It is possible that the blood-brain barrier is the initial site of damage that ultimately leads to inflammation in the brain that may produce some brain diseases. During stroke, thrombosis lodged in arteries leading to ischemia and reperfusion produces cell damage in many brain regions. This chapter will discuss mechanisms of adipokine and toxic lipid induced oxygen radical formation and damage to the blood-brain barrier. Active oxygen species such as hydrogen peroxide cross cell membranes, penetrate into the nucleus and very rapidly damage DNA. DNA peroxidation produces DNA fragments. DNA repair enzymes become activated and rapidly deplete cellular energy reserves, such as NAD and ATP. This drastically alters cell function and viability. Endothelial cell death makes the blood-brain barrier leak and may allow the infiltration of activated inflammatory cells that produce oxygen radicals that damage neurons and other brain cells. Neuronal death occurs through apoptosis and necrosis.
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Kumar Chatterjee, Swapan, Snigdha Saha, and Shahin Muhammed T.K. "COVID-19 and Its Impact on Onset and Progression of Parkinson’s and Cognitive Dysfunction." In COVID-19 Pandemic, Mental Health and Neuroscience - New Scenarios for Understanding and Treatment [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.105667.

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In the COVID-19 pandemic, neurological complications have emerged as a significant cause of morbidity and mortality. A wide range of neurological manifestations ranging from cognitive or memory disturbances, headache, loss of smell or taste, confusion, and disabling strokes have been reported during and post COVID conditions. The COVID-19 virus can utilize two possible pathways for invasion into the brain, either through retrograde axonal transport (olfactory route) or by crossing the blood-brain barrier (BBB). Furthermore, the production of SARS-CoV-2-associated cytokines, such as interleukin (IL)-6, IL-17, IL-1b, and tumor necrosis factor (TNF), is able to disrupt the BBB. The neuroinvasive nature of SARS-CoV-2 has a more severe impact on patients with preexisting neurological manifestations such as Parkinson’s disease (PD). Pathological features of PD include selective loss of dopaminergic neurons in the substantia nigra pars compacta and aggregation of α-syn proteins present in neurons. Interaction between SARS-COV-2 infection and α-synuclein might have long-term implications on the onset of Parkinsonism by the formation of toxic protein clumps called amyloid fibrils—a hallmark of Parkinson’s. Molecular modeling is an emerging tool to predict potential inhibitors against the enzyme α-synuclein in neurodegenerative diseases by using plant bioactive molecules.
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Hornedo-Ortega, Ruth, Zuriñe Rasines-Perea, Ana B. Cerezo, Pierre-Louis Teissedre, and Michael Jourdes. "Anthocyanins: Dietary Sources, Bioavailability, Human Metabolic Pathways, and Potential Anti-Neuroinflammatory Activity." In Phenolic Compounds - Chemistry, Synthesis, Diversity, Non-Conventional Industrial, Pharmaceutical and Therapeutic Applications. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.99927.

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The objectives of this chapter are to summarize and discuss (i) the anthocyanins structure and content in foodstuffs and their dietary intake (ii) the anthocyanins bioavailability and human metabolic pathways and (iii) the in vitro and in vivo potent anti-neuroinflammatory effects of anthocyanins and their metabolites. Indeed, anthocyanins are polyphenolic compounds belonging to the group of flavonoids, and are one of the most commonly consumed polyphenols in a normal diet. They are responsible of red, blue and purple color of several fruits and vegetables and their intake has been related with several human health benefits. The anthocyanins structures diversities as well as their content in various fruits, vegetables and cereals is addressed. Moreover, despite the growing evidence for the protective effects of anthocyanins, it is important to highlight that the in vivo bioavailability of these compounds is relatively low in comparison to their more stable metabolites. Indeed, after consumption, these bioactives are subjected to substantial transformations in human body. Phase I and II metabolites generated by intestinal and hepatic enzymatic reactions, and phenolic acids produced by gut microbiota and their metabolized forms, are the most important metabolic anthocyanins forms. For this reason, the study of the biological properties of these circulating metabolites represents a more in vivo realistic situation. Although the anthocyanin bioavailability researches in humans are limited, they will be discussed together with a global metabolic pathway for the main anthocyanins. Moreover, several works have demonstrated that anthocyanins can cross the blood brain barrier, and accumulate in brain endothelial cells, brain parenchymal tissue, striatum, hippocampus, cerebellum and cortex. Consequently, the study of anthocyanins as potent therapeutic agents in neurodegenerative diseases has gained relevance and the principal and the most recent studies are also discussed in the book chapter.
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Conference papers on the topic "Cadmium, blood-brain barrier, neurodegenerative diseases"

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Kim, Jung Hwan, Thomas H. Mareci, and Malisa Sarntinoranont. "Computational Model of Interstitial Transport in the Rat Brain Using Diffusion Tensor Imaging." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176633.

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Abstract:
In spite of the high therapeutic potential of macromolecular drugs, it has proven difficult to apply them to recovery after injury and treatment of cancer, Parkinson’s disease, and other neurodegenerative diseases. One barrier to systemic administration is low capillary permeability, i.e., the blood-brain and blood-spinal cord barrier. To overcome this barrier, convection-enhanced delivery (CED) infuses agents directly into tissue to supplement diffusion and increase the distribution of large molecules in the brain [1,2]. Predictive models of distribution during CED would be useful in treatment optimization and planning. To account for large infusion volumes, such models should incorporate tissue boundaries and anisotropic tissue properties.
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