Alzheimer's disease and multiple sclerosis: a possible connection through the viral demyelinating neurodegenerative

Marina S Boukhvalova1, Lorne Kastrukoff2, Jorge C G Blanco1

  • 1Sigmovir Biosystems, Inc., Rockville, MD, United States.

Insights

A proposed viral trigger model suggests early-life viral infections, like HSV-1, may cause demyelination leading to multiple sclerosis (MS) and later Alzheimer

Area of Science:

  • Neuroscience and Immunology
  • Infectious Diseases and Neurodegeneration

Background:

  • Alzheimer's disease (AD) and multiple sclerosis (MS) are prevalent CNS disorders lacking cures.
  • Current therapeutic approaches targeting amyloid or immune pathways have shown limited success, highlighting gaps in understanding disease etiology.
  • Growing evidence suggests infectious agents, particularly viruses, may play a role in neurodegenerative and demyelinating diseases.

Purpose of the Study:

  • To propose a unifying model, the viral DEmyelinating Neurodegenerative Trigger (vDENT), linking MS and AD through a common viral etiology and demyelination.
  • To explore how early-life viral infections could initiate a cascade leading to both MS and AD later in life.

Main Methods:

  • Conceptual model development (vDENT) based on existing evidence of viral infections, demyelination, and neurodegeneration.
  • Integration of known pathological mechanisms in MS (demyelination, inflammation) and AD (amyloid accumulation, neurodegeneration).
  • Hypothesizing the progression from initial demyelination to later-life AD dementia.

Main Results:

  • The vDENT model posits that initial demyelinating viral infections (e.g., HSV-1) trigger early-life demyelination.
  • Subsequent viral reactivations and inflammatory responses contribute to relapsing-remitting MS (RRMS).
  • Accumulated damage and viral progression, combined with age-related factors, promote amyloid dysfunction and AD dementia.

Conclusions:

  • Viral infections and subsequent demyelination may represent a shared pathway in the pathogenesis of both MS and AD.
  • Interventions targeting early-life viral events could potentially prevent or delay the onset of both MS and AD.
  • This model offers a new perspective for developing dual-benefit therapeutic strategies for these debilitating CNS disorders.

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