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      Formulations of Curcumin Nanoparticles for Brain Diseases

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          Abstract

          Curcumin is a polyphenol that is obtained from Curcuma longa and used in various areas, such as food and textiles. Curcumin has important anti-inflammatory and antioxidant properties that allow it to be applied as treatment for several emerging pathologies. Remarkably, there are an elevated number of publications deriving from the terms “curcumin” and “curcumin brain diseases”, which highlights the increasing impact of this polyphenol and the high number of study groups investigating their therapeutic actions. However, its lack of solubility in aqueous media, as well as its poor bioavailability in biological systems, represent limiting factors for its successful application. In this review article, the analysis of its chemical composition and the pivotal mechanisms for brain applications are addressed in a global manner. Furthermore, we emphasize the use of nanoparticles with curcumin and the benefits that have been reached as an example of the extensive advances in this area of health.

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          Most cited references102

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          Tau-mediated neurodegeneration in Alzheimer's disease and related disorders.

          Advances in our understanding of the mechanisms of tau-mediated neurodegeneration in Alzheimer's disease (AD) and related tauopathies, which are characterized by prominent CNS accumulations of fibrillar tau inclusions, are rapidly moving this previously underexplored disease pathway to centre stage for disease-modifying drug discovery efforts. However, controversies abound concerning whether or not the deleterious effects of tau pathologies result from toxic gains-of-function by pathological tau or from critical losses of normal tau function in the disease state. This Review summarizes the most recent advances in our knowledge of the mechanisms of tau-mediated neurodegeneration to forge an integrated concept of those tau-linked disease processes that drive the onset and progression of AD and related tauopathies.
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            Neuroinflammation: the devil is in the details.

            There is significant interest in understanding inflammatory responses within the brain and spinal cord. Inflammatory responses that are centralized within the brain and spinal cord are generally referred to as 'neuroinflammatory'. Aspects of neuroinflammation vary within the context of disease, injury, infection, or stress. The context, course, and duration of these inflammatory responses are all critical aspects in the understanding of these processes and their corresponding physiological, biochemical, and behavioral consequences. Microglia, innate immune cells of the CNS, play key roles in mediating these neuroinflammatory responses. Because the connotation of neuroinflammation is inherently negative and maladaptive, the majority of research focus is on the pathological aspects of neuroinflammation. There are, however, several degrees of neuroinflammatory responses, some of which are positive. In many circumstances including CNS injury, there is a balance of inflammatory and intrinsic repair processes that influences functional recovery. In addition, there are several other examples where communication between the brain and immune system involves neuroinflammatory processes that are beneficial and adaptive. The purpose of this review is to distinguish different variations of neuroinflammation in a context-specific manner and detail both positive and negative aspects of neuroinflammatory processes. In this review, we will use brain and spinal cord injury, stress, aging, and other inflammatory events to illustrate the potential harm and benefits inherent to neuroinflammation. Context, course, and duration of the inflammation are highly important to the interpretation of these events, and we aim to provide insight into this by detailing several commonly studied insults. This article is part of the 60th anniversary supplemental issue.
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              Alzheimer's disease: strategies for disease modification.

              Alzheimer's disease is the largest unmet medical need in neurology. Current drugs improve symptoms, but do not have profound disease-modifying effects. However, in recent years, several approaches aimed at inhibiting disease progression have advanced to clinical trials. Among these, strategies targeting the production and clearance of the amyloid-beta peptide - a cardinal feature of Alzheimer's disease that is thought to be important in disease pathogenesis - are the most advanced. Approaches aimed at modulating the abnormal aggregation of tau filaments (another key feature of the disease), and those targeting metabolic dysfunction, are also being evaluated in the clinic. This article discusses recent progress with each of these strategies, with a focus on anti-amyloid strategies, highlighting the lessons learned and the challenges that remain.
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                Author and article information

                Journal
                Biomolecules
                Biomolecules
                biomolecules
                Biomolecules
                MDPI
                2218-273X
                08 February 2019
                February 2019
                : 9
                : 2
                : 56
                Affiliations
                [1 ]Laboratorio de Posgrado en Tecnología Farmacéutica, FES-Cuautitlán, Universidad Nacional Autónoma de México, Cuautitlán Izcalli 54740, Mexico; ml.delprado@ 123456iim.unam.mx
                [2 ]Departamento de Fisiología, Biofísica & Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México 07360, Mexico; hiram.qfohead@ 123456gmail.com (I.H.C.-F.); bfloran@ 123456fisio.cinvestav.mx (B.F.)
                [3 ]Departamento de Farmacia, Facultad de Química, Universidad Nacional Autónoma de México, Ciudad Universitaria, Circuito Exterior S/N, Del. Coyoacán, C.P. Ciudad de México 04510, Mexico; jamtoledo90@ 123456outlook.com
                [4 ]Escuela de Ciencias de la Salud, Universidad del Valle de México, Campus Coyoacán, Ciudad de México, 04910, Mexico
                [5 ]Facultad de Ciencias Químicas, Universidad de Colima, C.P. Colima 28400, México; nmendoza0@ 123456ucol.cmx
                [6 ]CONACyT-Laboratorio de Biotecnología, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Ciudad de México 14389, Mexico; mikegcu@ 123456gmail.com
                [7 ]Instituto Tecnológico y de Estudios Superiores de Monterrey, Campus Ciudad de México 14380, Mexico
                [8 ]Laboratorio de Medicina Genómica, Departamento de Genética, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Ciudad de México 14389, Mexico
                Author notes
                [* ]Correspondence: hcortes@ 123456inr.gob.mx or hcortes_c@ 123456hotmail.com (H.C.); gerardoleyva@ 123456hotmail.com (G.L.-G.); Tel.: +52-55-59991000 (ext. 14710) (H.C.); +52-55-56223899 (ext. 44408) (G.L.-G.)
                Author information
                https://orcid.org/0000-0003-2252-6997
                https://orcid.org/0000-0003-3899-4410
                https://orcid.org/0000-0002-3430-9335
                https://orcid.org/0000-0002-6147-4109
                Article
                biomolecules-09-00056
                10.3390/biom9020056
                6406762
                30743984
                f6179591-b758-4674-b22c-cf31eff84b40
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 14 December 2018
                : 01 February 2019
                Categories
                Review

                curcumin,nanoparticles,inflammation,protein aggregation,brain diseases,alzheimer’s disease,parkinson’s disease

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