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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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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Ciencia básica y patogénesis

Mayank Pushpam1,2, Rehab Hussain2, Latha Diwakar2

  • 1Manipal Academy of Higher Education, Manipal, Karnataka, India.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
PubMed
Resumen
Este resumen es generado por máquina.

Las lesiones vasculares empeoran el Alzheimer

Palabras clave:
Enfermedad de AlzheimerPatología vascularBarrera hematoencefálicaNeuroinflamaciónPleiotrofinaModelos de ratónEndotelina-1

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Área de la Ciencia:

  • Neurociencia; Biología Vascular; Investigación de la Enfermedad de Alzheimer

Sus antecedentes:

  • La enfermedad de Alzheimer (EA) a menudo se presenta como demencia mixta con patología vascular, particularmente en ancianos.; Los factores de riesgo vascular se relacionan con cambios en la sustancia blanca y el deterioro cognitivo, exacerbando la patología de amiloide-β (Aβ) y tau en la EA.; Este estudio investiga los cambios en la barrera hematoencefálica (BHE) y la neuroinflamación en relación con la formación de placas de Aβ y los déficits cognitivos en modelos de EA.

Objetivo del estudio:

  • Investigar los mecanismos moleculares de la patología vascular, incluidos los cambios en la barrera hematoencefálica (BHE) y la neuroinflamación, en la enfermedad de Alzheimer (EA).; Evaluar el impacto de las lesiones vasculares en la formación de placas de amiloide-β (Aβ) y los déficits cognitivos en modelos de ratón transgénico de EA.; Evaluar los efectos protectores de los factores tróficos, específicamente la pleiotrofina (PTN), contra las lesiones vasculares y la disfunción de la BHE en la EA.

Principales métodos:

  • Se utilizaron ratones transgénicos con enfermedad de Alzheimer (EA) (modelos APPswe y J20).; Se indujo lesión vascular mediante inyección de endotelina-1 (ET-1) en los ventrículos laterales.; Se evaluó la integridad de la barrera hematoencefálica (BHE), la neuroinflamación y la función cognitiva mediante inmunohistoquímica y pruebas de comportamiento. Se utilizó pleiotrofina (PTN) para la evaluación del efecto protector.

Principales resultados:

  • La endotelina-1 (ET-1) indujo déficits de memoria y ruptura de la barrera hematoencefálica (BHE) en ratones APPswe, caracterizada por infiltración de macrófagos y neuroinflamación.; Se observó un aumento de la activación microglial tanto en los modelos de ratón APPswe como J20 de EA, lo que se correlaciona con una mayor deposición de placas en los ratones J20.; El factor trófico pleiotrofina (PTN) demostró un efecto protector al prevenir la disrupción de la BHE inducida por ET-1 en ratones APPswe.

Conclusiones:

  • Las lesiones vasculares afectan de manera diferente a los modelos de ratón de EA (APPswe vs. J20) en cuanto a susceptibilidad y cambios en la integridad de la BHE, variando con la edad.; El estudio destaca el papel de la patología vascular y la neuroinflamación en la exacerbación de la progresión de la EA.; La pleiotrofina (PTN) muestra potencial como agente terapéutico al prevenir la disfunción de la BHE en el contexto de las lesiones vasculares relacionadas con la EA.