Fundamental immunological problems associated with "transmissible spongiform encephalopathies".

Area of Science:

• Neurology
• Infectious Diseases
• Veterinary Medicine

Background:

• Transmissible spongiform encephalopathies (TSEs) include Bovine Spongiform Encephalopathy (BSE), scrapie, Creutzfeldt-Jakob disease, and kuru.
• Current diagnostic methods rely on LD50 measurements and autopsy, assuming saline brain homogenates are non-damaging.
• This assumption is challenged by known inflammatory responses to brain homogenates, such as post-rabies vaccination allergic encephalomyelitis.

Purpose of the Study:

• To identify fundamental flaws in the diagnostic assumptions for transmissible spongiform encephalopathies.
• To propose an alternative diagnostic approach by examining infectious agents with potential roles in TSE pathogenesis.
• To investigate the link between Acinetobacter, molecular mimicry with myelin, and TSEs.

Main Methods:

• Critically evaluate the assumption of non-pathogenicity of saline brain homogenates in TSE diagnosis.
• Examine infectious agents, specifically Acinetobacter, for molecular mimicry with host tissues like myelin.
• Analyze antibody levels against Acinetobacter in animal models of BSE and human patients with multiple sclerosis.

Main Results:

• The standard diagnostic approach for TSEs is based on an untenable assumption of non-pathogenicity of injected brain homogenates.
• Acinetobacter exhibits molecular mimicry with myelin, a key component of nervous tissue.
• Elevated antibodies against Acinetobacter are observed in animals with BSE and in multiple sclerosis patients.

Conclusions:

• The fundamental diagnostic flaw in TSEs lies in the assumption regarding brain homogenates.
• Infectious agents like Acinetobacter, through molecular mimicry, present a promising avenue for further research and potential diagnostic development for TSEs and related conditions like multiple sclerosis.