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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.
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Urinary Tract Infection II: Pathophysiology01:25

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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

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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.
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Pneumonia II: Pathophysiology01:29

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Stages of Infection01:26

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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

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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.
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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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Ciencia básica y patogénesis

Sandra O Tomé1, Klara Gawor1, Christine A F von Arnim2

  • 1Laboratory of Neuropathology, KU Leuven, Leuven, Vlaams-Brabant, Belgium.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 28, 2025
PubMed
Resumen
Este resumen es generado por máquina.

La proteinopatía TDP-43 difiere entre la encefalopatía por TDP-43 relacionada con la edad predominante en el lóbulo límbico (LATE) y la coinfección de la enfermedad de Alzheimer (AD). El LATE puro muestra patrones distintos de lesiones de TDP-43, lo que sugiere diferentes mecanismos de agregación en la demencia.

Palabras clave:
Encefalopatía por TDP-43 relacionada con la edad predominante en el lóbulo límbicoEnfermedad de AlzheimerCoinfecciónMorfología de las lesionesAgregación de proteínasNeuropatologíaDemencia

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Área de la Ciencia:

  • Neuropatología
  • Neurociencia
  • Medicina Geriátrica

Sus antecedentes:

  • La encefalopatía por TDP-43 relacionada con la edad predominante en el lóbulo límbico (LATE) es una causa de demencia recientemente identificada.
  • LATE y la enfermedad de Alzheimer (AD) comparten síntomas clínicos y a menudo coexisten neuropatológicamente.
  • La morfología de las lesiones de TDP-43 en la demencia requiere una mayor investigación.

Objetivo del estudio:

  • Investigar la morfología de las lesiones de TDP-43 y las especies inmunorreactivas en LATE puro y en casos con cambios neuropatológicos coexistentes de AD (ADNC).
  • Diferenciar las características histopatológicas de la proteinopatía por TDP-43 en LATE-NC versus ADNC+LATE-NC.

Principales métodos:

  • Inmunohistoquímica en tejido cerebral post mortem humano (hipocampo, amígdala, cortezas) de 70 casos.
  • Evaluación semicuantitativa de inclusiones citoplasmáticas neuronales (ICN) y neuritas distróficas (ND) de TDP-43.
  • Análisis de varias especies de TDP-43 (pS409/410, pS409/pS403, pS403/pS404, TDP-43 C- y N-terminal).

Principales resultados:

  • Los casos puros de LATE-NC mostraron predominantemente un patrón en banda de neuritas distróficas en el hipocampo.
  • Los casos puros de LATE-NC tuvieron una carga más severa de neuritas distróficas en el hipocampo, la amígdala y la corteza temporal en comparación con ADNC+LATE-NC.
  • Los casos ADNC+LATE-NC exhibieron una mayor predominancia de inclusiones citoplasmáticas neuronales en la amígdala y perfiles distintos de especies de TDP-43.

Conclusiones:

  • Las características histopatológicas de la proteinopatía por TDP-43 difieren entre LATE-NC puro y ADNC coexistente.
  • LATE-NC parece estar modificado por la presencia de niveles moderados a altos de ADNC.
  • Mecanismos distintos pueden subyacer a la agregación de TDP-43 en diferentes demencias, y las patologías coexistentes se influyen mutuamente.