Vascular malformations are frequent in the head and neck region, affecting the nervous system. The wide range of therapeutic approaches demand the correct anatomical, morphological, and functional characterization of these lesions supported by imaging. Using a systematic search protocol in PubMed, Google Scholar, Ebsco, Redalyc, and SciELO, the authors extracted clinical studies, review articles, book chapters, and case reports that provided information about vascular cerebral malformations, in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A total of 385,614 articles were grouped; using the inclusion and exclusion criteria, three of the authors independently selected 51 articles about five vascular cerebral malformations: venous malformation, brain capillary telangiectasia, brain cavernous angiomas, arteriovenous malformation, and leptomeningeal angiomatosis as part of Sturge–Weber syndrome. We described the next topics—“definition”, “etiology”, “pathophysiology”, and “treatment”—with a focus on the relationship with the imaging approach. We concluded that the correct anatomical, morphological, and functional characterization of cerebral vascular malformations by means of various imaging studies is highly relevant in determining the therapeutic approach, and that new lines of therapeutic approaches continue to depend on the imaging evaluation of these lesions.
Parkinson’s disease is a neurodegenerative disease whose progression and clinical characteristics have a close bidirectional and multilevel relationship with the process of neuroinflammation. In this context, it is necessary to understand the mechanisms involved in this neuroinflammation–PD link. This systematic search was, hereby, conducted with a focus on the four levels where alterations associated with neuroinflammation in PD have been described (genetic, cellular, histopathological and clinical-behavioral) by consulting the PubMed, Google Scholar, Scielo and Redalyc search engines, including clinical studies, review articles, book chapters and case studies. Initially, 585,772 articles were included, and, after applying the inclusion and exclusion criteria, 84 articles were obtained that contained information about the multilevel association of neuroinflammation with alterations in gene, molecular, cellular, tissue and neuroanatomical expression as well as clinical-behavioral manifestations in PD.
Considered a neurodegenerative disease, Alzheimer's disease (AD) involves a physiopathological process characterized by the presence of the beta-amyloid peptide, hyperphosphorylated Tau protein, and neuroinflammation. Diabetes mellitus (DM) is an endocrine disease characterized by insulin resistance, where decreased production of this hormone causes a constant state of hyperglycemia. Although it is recognized that DM is a risk factor for the development of AD, the compression of the mechanisms involved is not completely understood. The present review evaluates the information acquired from primary and secondary sources, focusing on the alterations in gene expression associated with AD as well as the alterations in gene expression associated with DM, to later highlight the influence that these types of alterations developed in patients with DM can have on both the development and progression of AD. Finally, we point out those alterations that impact the phosphatidyl Inositol 3 Kinase/Akt (PI3K/Akt) pathway, which seems to intervene in the physiopathological process of both diseases, considering that the compression of these gene alterations can help us understand the intricate link between DM and AD.
Entre la Enfermedad de Alzheimer (EA) y la Diabetes Mellitus (DM) ha sido evidenciado que existen múltiples mecanismos en común en ambas patologías, que van desde el deterioro cognitivo en el aspecto clínico hasta alteraciones bioquímicas de las cuales destacan; el aumento de los agentes proinflamatorios y la excitotoxicidad, aumento del estrés oxidativo y aumento de los productos finales de la glicación avanzada (AGEs), alteraciones del metabolismo de la glucosa, así como alteraciones de las vías mTORC1 /S6 y GSK-3 β; así también destaca el papel de la Resistencia a la Insulina (Ri), donde esta alteración está vinculada tanto con EA como con DM en diversos puntos de su fisiopatología, ya sea mediante la influencia en los diferentes mecanismos antes mencionados o bien de forma directa. Objetivo. Se describe como la influencia de esta hormona es tal, tanto si sus niveles son altos, efecto conocido como hiperinsulinismo o bajos efecto conocido como hipoinsulinismo, puesto que ambos extremos conducen a efectos neurodegenerativos característicos de EA, principalmente en el aumento de β amiloide (Aβ) y Tau hiperfosforilada (pTau), a través de distintos procesos. Aporte.Es con base en este fenómeno que nosotros describimos lo que llamamos “La paradoja de la insulina”, en la cual además destaca la vía insulina/PI3K/Akt como punto crucial, ya que independientemente de las condiciones de hiper o hipoinsulinismo esta vía se altera en ambos escenarios. Esta relación entre EA y DM se considera desde el aspecto de los tratamientos hipoglucemiantes dirigidos a la atención de DM, los cuales parecen interferir con EA, a través de varios de los mecanismos en común que tienen estas patologías. Conclusión. Aunque es muy prematuro considerar que estos tratamientos para DM darán los mismos resultados en los casos de EA, estos datos son valiosos precedentes en la búsqueda de alternativas terapéuticas para EA.
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