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Infection01:20

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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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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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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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Basic Science and Pathogenesis.

Mohammad Walid1, Haneen Beshr El-Alfy1, Rahma Mohammed Ibrahim1

  • 1Faculty of Medicine, Arish University, Arish, North Sinai, Egypt.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease pathogenesis involves neuroinflammation, not just amyloid-beta and tau. Early-onset AD stems from immune hyperactivity, while late-onset AD results from immunosenescence, with both converging on protein deposition.

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Early-onset Alzheimer's disease (EOAD) pathogenesis is not fully understood, and current therapies are ineffective.
  • Traditional models focusing solely on amyloid-beta (Aβ) and tau may be incomplete.
  • Investigating alternative mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To re-evaluate Alzheimer's disease (AD) pathogenesis, focusing on the role of neuroinflammation.
  • To differentiate the underlying mechanisms of early-onset AD (EOAD) and late-onset AD (LOAD).
  • To identify novel therapeutic targets by understanding the immune system's role in AD.

Main Methods:

  • Comprehensive literature review of MEDLINE, PsycINFO, and Cochrane Central Register up to January 2025.
  • Analysis of genetic and protein databases.
  • Molecular studies using human-induced neural stem cells (hiNSCs) to model AD pathology.

Main Results:

  • Neuroimmune dysregulation is central to AD pathogenesis, preceding or exceeding Aβ and tau roles.
  • Traumatic brain injury (TBI) and pathogens (e.g., HSV-1) activate innate immunity, inducing Aβ/tau pathology via pattern recognition receptors (PRRs).
  • EOAD involves genetic susceptibility and environmental triggers leading to astrocytic immune hyperactivity, while LOAD involves aging-related immunosenescence impairing clearance. Aβ acts as an antimicrobial peptide, but overproduction drives pathology.

Conclusions:

  • AD heterogeneity arises from distinct immune-driven pathways: hyperimmune state in EOAD and immunosenescence in LOAD.
  • Both EOAD and LOAD converge on Aβ and tau deposition as downstream consequences.
  • Innate immunity plays a central role in AD pathogenesis, offering new targets for immune modulation therapies.