Jove
Visualize
Contáctanos

Videos de Conceptos Relacionados

Infection01:20

Infection

11.6K
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...
11.6K
Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

524
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...
524
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

676
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,...
676
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

2.5K
The pathophysiology of pneumonia involves the following steps:
2.5K
Stages of Infection01:26

Stages of Infection

64.7K
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...
64.7K
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

2.6K
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...
2.6K

También podría leer

Artículos Relacionados

Artículos vinculados a este trabajo por autores compartidos, revista y gráfico de citas.

Ordenar por
Same author

Altered theta-band sensory gating in individuals with high sensory processing sensitivity (SPS).

Brain research·2026
Same author

Resveratrol isomers with opposing activities target endonuclease G to modulate neurodegeneration and mitochondrial elimination.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Predicting the timing of first sustained cognitive worsening in Alzheimer's disease using real-world clinical data and machine learning.

medRxiv : the preprint server for health sciences·2026
Same author

Expansion Revealing of Pathology Resolves Nanostructures Associated with Inflammatory Phenotypes in COVID-19 Decedent Human Brain Tissue.

bioRxiv : the preprint server for biology·2026
Same author

DNA double-strand break signaling induces aberrant neuronal activity.

bioRxiv : the preprint server for biology·2026
Same author

Loss-of-Function (G603R) Lrp10 Fails to Downregulate mRNA of Pathologic α-Synuclein and Causes Neurodegeneration of Substantia Nigra Dopaminergic Cells in Parkinson's Disease Knockin Mice.

Neurochemical research·2026
Same journal

Multimorbidity burden and patterns associated with DeepBrainNet-derived brain-age gap in dementia-free older adults: A community-based study.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

Reply to "Shifting the emphasis of brain health literacy from individuals to systems to reduce inequalities".

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

Shifting the emphasis of brain health literacy from individuals to systems to reduce inequalities.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

Correlates and predictors of self-efficacy among dementia caregivers: D-CARE findings.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

What should convince a clinician of disease modification in Alzheimer's disease clinical trials?

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

Primary cilia-extracellular vesicle crosstalk in Alzheimer's disease: Emerging mechanisms and biomarker potential.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Ver todos los artículos relacionados
JoVE
x logofacebook logolinkedin logoyoutube logo
ACERCA DE JoVE
Visión GeneralLiderazgoBlogCentro de Ayuda JoVE
AUTORES
Proceso de PublicaciónConsejo EditorialAlcance y PolíticasRevisión por ParesPreguntas FrecuentesEnviar
BIBLIOTECARIOS
TestimoniosSuscripcionesAccesoRecursosConsejo Asesor de BibliotecasPreguntas Frecuentes
INVESTIGACIÓN
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchivo
EDUCACIÓN
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualCentro de Recursos para ProfesoresSitio de Profesores
Términos y Condiciones de Uso
Política de Privacidad
Políticas

Video Experimental Relacionado

Updated: Jan 8, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
09:07

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses

Published on: June 14, 2020

11.5K

Ciencia básica y patogénesis

Djuna K Von Maydell1, Shannon Wright1, Colin Staab1

  • 1Massachusetts Institute of Technology, Cambridge, MA, USA.

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

Las variantes genéticas en ABCA7 alteran el metabolismo de los lípidos y la función mitocondrial, lo que contribuye al riesgo de la enfermedad de Alzheimer. El tratamiento con CDP-colina muestra la promesa de restaurar la función y reducir la patología.

Palabras clave:
ABCA7Enfermedad de Alzheimermetabolismo lipídicofunción mitocondrialCDP-colinaneurocienciagenéticabioquímica

Más Videos Relacionados

A Precise Pathogen Delivery and Recovery System for Murine Models of Secondary Bacterial Pneumonia
13:45

A Precise Pathogen Delivery and Recovery System for Murine Models of Secondary Bacterial Pneumonia

Published on: September 21, 2019

6.0K
Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
08:38

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Published on: February 22, 2019

6.3K

Videos de Experimentos Relacionados

Last Updated: Jan 8, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
09:07

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses

Published on: June 14, 2020

11.5K
A Precise Pathogen Delivery and Recovery System for Murine Models of Secondary Bacterial Pneumonia
13:45

A Precise Pathogen Delivery and Recovery System for Murine Models of Secondary Bacterial Pneumonia

Published on: September 21, 2019

6.0K
Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
08:38

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Published on: February 22, 2019

6.3K

Área de la Ciencia:

  • Neurociencia; Genética; Bioquímica

Sus antecedentes:

  • Las variantes raras de pérdida de función en el transportador de lípidos ABCA7 son factores de riesgo genético significativos para la enfermedad de Alzheimer (EA).
  • Comprender los mecanismos que vinculan las variantes de ABCA7 con el riesgo de EA es crucial para el desarrollo de terapias.

Objetivo del estudio:

  • Investigar los mecanismos moleculares por los cuales las variantes de pérdida de función de ABCA7 contribuyen a la enfermedad de Alzheimer.
  • Explorar la relevancia de estos hallazgos para una población más amplia en riesgo.

Principales métodos:

  • Secuenciación de ARN de núcleo único en muestras de cerebro de portadores de variantes de ABCA7 y controles.
  • Análisis de datos post mortem de portadores de una variante común de ABCA7 que confiere riesgo de EA.
  • Simulaciones de dinámica molecular y estudios funcionales utilizando neuronas derivadas de células madre pluripotentes inducidas (iPSC).

Principales resultados:

  • ABCA7 se expresa en altos niveles en neuronas excitatorias, donde sus variantes alteran el metabolismo de los lípidos, la función mitocondrial y la señalización sináptica.
  • Los cambios transcripcionales en portadores de variantes se superponen con los relacionados con una variante común de ABCA7 que confiere riesgo de EA.
  • Las neuronas con pérdida de función de ABCA7 exhiben acumulación de triglicéridos, alteración del metabolismo de la fosfatidilcolina y deterioro de la función mitocondrial.
  • El tratamiento con CDP-colina restauró la función mitocondrial, revirtió los defectos transcripcionales y redujo la patología de amiloide-beta.

Conclusiones:

  • La alteración de la fosfatidilcolina está implicada en los defectos metabólicos y patológicos asociados con la disfunción de ABCA7 en la enfermedad de Alzheimer.
  • Estos hallazgos resaltan el papel de la disfunción lipídica en la etiología de la EA y sugieren posibles estrategias terapéuticas dirigidas al metabolismo de la fosfatidilcolina.