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Simultaneous Cryosectioning of Multiple Rodent Brains
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Fortress brain.

Donald R Royall1

  • 1Department of Psychiatry, The University of Texas Health Science Center, San Antonio, TX, USA. royall@uthscsa.edu

Medical Hypotheses
|December 26, 2012
PubMed
Summary
This summary is machine-generated.

Neurodegenerative diseases like Alzheimer's Disease (AD) and Lewy Body Disease (LBD) may originate from infectious agents, spreading through neural pathways. The brain may have evolved defense mechanisms against these neurotropic pathogens.

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10:35

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Published on: January 12, 2020

Area of Science:

  • Neuroscience
  • Pathology
  • Infectious Diseases

Background:

  • Neurodegenerative diseases feature protein aggregates in neurons.
  • Alzheimer's Disease (AD) and Lewy Body Disease (LBD) show hierarchical, retrograde transynaptic lesion patterns.
  • This pattern suggests a temporal propagation, hinting at infectious origins.

Purpose of the Study:

  • To explore the hypothesis that AD and LBD have infectious origins.
  • To investigate the implications of transynaptic infiltration of the central nervous system (CNS) by infectious agents.
  • To re-evaluate the evolutionary adaptations of the human brain against neurotropic pathogens.

Main Methods:

  • Analysis of lesion distribution patterns in AD and LBD.
  • Inference of propagation mechanisms based on spatial and temporal patterns.
  • Consideration of host-parasite interactions and evolutionary perspectives.

Main Results:

  • The spatial pattern of lesions in AD and LBD suggests retrograde transynaptic spread.
  • Infectious agents are proposed as a primary explanation for this propagation.
  • The clinical presentation of neurodegenerative disorders may depend on the infectious agent's entry point.

Conclusions:

  • AD and LBD may have infectious etiologies, spreading via neural pathways.
  • The human brain may possess evolved defense mechanisms, such as antimicrobial protein properties and structural barriers, against neurotropic invaders.
  • Understanding these mechanisms could redefine the approach to neurodegenerative diseases.