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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.
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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
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Updated: Jan 8, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Haishan Jiao1

  • 1Huashan Hospital, Fudan University, Shanghai, Shanghai, China.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary

Genetic variations in MS4A6A influence Alzheimer's disease (AD) risk. This study found that MS4A6A deficiency impairs brain repair mechanisms, suggesting boosting MS4A6A could be a novel AD treatment.

Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Genetic variations in MS4A6A are linked to Alzheimer's disease (AD) risk.
  • Previous studies suggest MS4A6A expression correlates with AD neuropathology severity.
  • The precise mechanisms of MS4A6A in AD pathogenesis are not well understood.

Purpose of the Study:

  • To investigate the role of MS4A6A in Alzheimer's disease pathogenesis.
  • To explore the functional impact of MS4A6A genetic variations on AD risk and biomarkers.
  • To elucidate the molecular mechanisms by which MS4A6A influences neuroinflammation and amyloid pathology.

Main Methods:

  • Conducted a meta genome-wide association analysis of MS4A6A polymorphisms with AD risk in 734,121 subjects.
  • Correlated MS4A6A levels with cerebrospinal fluid AD biomarkers in a human cohort.

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  • Generated and analyzed a Ms4a6d deficient APP/PS1 mouse model using microscopy, biochemistry, and behavioral tests.

    • Main Results:

    • Identified novel MS4A6A mutations associated with AD risk and altered cerebrospinal fluid β-amyloid levels.
    • Ms4a6d deficiency in APP/PS1 mice impaired microglial amyloid clearance, increased plaque burden, and worsened synaptic damage.
    • Ms4a6d deficiency exacerbated neuroinflammation via dysregulation of the NF-κB pathway in microglia and astrocytes.

    Conclusions:

    • Ms4a6d deficiency compromises neuroprotection and exacerbates neuroinflammation in an AD model.
    • Elevated MS4A6A levels in AD patients may be a compensatory response.
    • Therapeutically boosting MS4A6A presents a potential treatment strategy for Alzheimer's disease.