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Infection01:20

Infection

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
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Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

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The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
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Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
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Pneumonia II: Pathophysiology01:29

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The pathophysiology of pneumonia involves the following steps:
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Stages of Infection01:26

Stages of Infection

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Stages of infection describe what happens to a susceptible host once a pathogen invades the human body. The stages of infection are incubation, prodromal, illness, stage of decline, and convalescence. The incubation stage is the period from exposure to a pathogen until symptoms start. The infected person is unaware of impending illness as the pathogens grow and multiply within the body. The duration may vary depending on the type of infection. The incubation period of measles averages ten to...
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Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
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Video Experimental Relacionado

Updated: Jan 7, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses

Published on: June 14, 2020

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Ciencia básica y patogénesis

Silvia Fossati1

  • 1Alzheimer's Center at Temple, Lewis Katz School of Medicine, Philadelphia, PA, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
PubMed
Resumen
Este resumen es generado por máquina.

La enfermedad de Alzheimer y la patología tau cambian las células endoteliales del cerebro hacia la glucólisis, aumentando la inflamación y la permeabilidad de la barrera hematoencefálica. La restauración del metabolismo normal revierte estos efectos perjudiciales, ofreciendo nuevas dianas terapéuticas.

Palabras clave:
enfermedad de Alzheimerproteína taubarrera hematoencefálicacélulas endotelialesmetabolismoinflamaciónpermeabilidadglucólisisangiopatía amiloide cerebralneurodegeneración

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Área de la Ciencia:

  • Neurociencia
  • Biología celular
  • Bioquímica

Sus antecedentes:

  • Las células endoteliales cerebrales (cECs) son cruciales para la integridad de la barrera hematoencefálica (BHE) y la función de la unidad neurovascular.
  • La disfunción de las cECs contribuye a la neuroinflamación, la neurodegeneración y las microhemorragias observadas en la enfermedad de Alzheimer (AD) y la angiopatía amiloide cerebral (CAA).
  • Los agregados patológicos de amiloide-beta (Aβ) y tau alteran el metabolismo de las cECs, promoviendo la glucólisis y alterando la función mitocondrial, lo que está relacionado con la permeabilidad de la BHE.

Objetivo del estudio:

  • Investigar los mecanismos por los cuales la patología de AD y CAA altera la función de las cECs.
  • Comprender cómo la disfunción de las cECs media las alteraciones de la BHE y la neurovascular.
  • Explorar el vínculo entre los cambios metabólicos en las cECs y la activación inflamatoria endotelial y la permeabilidad de la BHE.

Principales métodos:

  • Se evaluó la respiración mitocondrial y la glucólisis en cECs humanas utilizando el analizador de flujo extracelular Seahorse.
  • Se midió la función de la BHE a través de la resistencia eléctrica transendotelial (TEER) utilizando el sistema ECIS Zθ.
  • Se cuantificó la activación inflamatoria endotelial y las vías de disfunción vascular utilizando el panel de neuroinflamación MSD V-Plex, Western Blot e inmunofluorescencia.
  • Se investigaron los efectos de la inhibición de la glucólisis en la disfunción de la BHE y la neurovascular in vitro y en modelos animales de amiloidosis cerebral y taupatía.

Principales resultados:

  • Tanto los agregados de Aβ como los de tau inducen un cambio metabólico hacia la glucólisis en las cECs, lo que conduce a la activación inflamatoria y a la permeabilidad de la BHE.
  • La reducción de la glucólisis a niveles normales puede revertir los efectos cerebrovasculares perjudiciales causados por los agregados patológicos de AD.
  • El Aβ cambia directamente las cECs de la respiración mitocondrial a la glucólisis, mientras que el tau hiperactiva inicialmente la glucólisis, causando inflamación y permeabilidad de la BHE, seguido de disfunción mitocondrial y muerte celular.
  • Los hallazgos clave se confirmaron en modelos animales de amiloidosis cerebral y taupatía.

Conclusiones:

  • Se ha identificado un nuevo mecanismo metabólico que implica la activación inflamatoria endotelial y la patología de la BHE mediada por especies de Aβ y tau.
  • La modulación de esta vía metabólica presenta posibles estrategias terapéuticas para la AD, la CAA y las taupatías.
  • Las intervenciones dirigidas a normalizar el metabolismo endotelial podrían limitar la infiltración de células inmunitarias y la permeabilidad de la BHE en enfermedades neurodegenerativas.