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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

Pneumonia II: Pathophysiology

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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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Updated: Jan 8, 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

Chinaza Lilian Dibia1,2, Nathalie Vacaresse2, Rikke Han Kofoed3

  • 1University of Toronto, Toronto, ON, Canada.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
PubMed
Resumen

Este estudio muestra que el promotor del ácido fibrilar glial (GFAP) puede regular la terapia génica en modelos de la enfermedad de Alzheimer. Este enfoque aprovecha los astrocitos reactivos para controlar la producción de anticuerpos terapéuticos para un posible tratamiento en todo el cerebro.

Palabras clave:
ácido fibrilar glialpromotorterapia génicaenfermedad de AlzheimerastrocitosAAVbeta amiloideanticuerposneurocienciamodelos de ratón

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Área de la Ciencia:

  • Neurociencia
  • Terapia génica
  • Investigación de la enfermedad de Alzheimer

Sus antecedentes:

  • Los virus adenoasociados recombinantes (AAV) como AAV.PHP.eB pueden cruzar la barrera hematoencefálica.
  • Se investigan anticuerpos dirigidos contra péptidos beta amiloides (Aβ) para la inmunoterapia génica de la enfermedad de Alzheimer (EA).
  • La actividad del promotor del ácido fibrilar glial (GFAP) aumenta con la patología Aβ, ofreciendo un mecanismo regulador potencial.

Objetivo del estudio:

  • Determinar si los astrocitos reactivos pueden regular la expresión de anticuerpos anti-Aβ utilizando el promotor GFAP.
  • Evaluar la eficacia de la entrega de genes mediada por AAV y la función del promotor GFAP en un modelo de ratón de amiloidosis.

Principales métodos:

  • Se cuantificaron los niveles de ARNm de GFAP en ratones TgCRND8 (Tg) en diferentes edades utilizando qPCR.
  • Se coinyectaron vectores AAV que codifican un anticuerpo anti-Aβ (rSol) o GFP bajo el promotor GFAP en ratones Tg.
  • Se analizaron secciones cerebrales utilizando inmunohistoquímica y RNAscope para evaluar la expresión génica y la transducción.

Principales resultados:

  • Los niveles de ARNm de GFAP aumentaron con la edad en ratones Tg.
  • La expresión de GFP en todo el cerebro confirmó la actividad del promotor GFAP en astrocitos.
  • La eficiencia de transducción varió entre los ratones Tg, potencialmente debido a los niveles de proteína Ly6A que influyen en la entrada de AAV.PHP.eB.

Conclusiones:

  • El promotor GFAP puede controlar potencialmente la producción terapéutica en respuesta a la reactividad astrocítica inducida por amiloide.
  • Se necesitan estudios a largo plazo adicionales para evaluar si rSol puede prevenir la progresión de la patología Aβ en modelos de ratón de EA.