Reasonable, простите, но в этой статье не выдвигается версия о том, что болезнь Альцгеймера вызвана хронической инфекцией, - об этом говорилось раньше. Здесь просто доказывается, что бета-амилоид является антимикробным агентом. Также говорится о генетических поломках (упомянуты). Уж простите.
С уважением,
Улька
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And in a third mechanism, an inappropriate inflammatory response by the innate immune system to transient or persistent non-infectious insults could also trigger a self-perpetuating innate immune response. While dozens of diseases have been suggested to involve immune abnormalities, for most, the underlying cause of the aberrant immunoresponse remains unclear. For AD, traumatic brain injury [71], stroke [72] and certain forms of inhalant anesthetics [73] have been linked to increased cerebral Aβ levels. Thus, while an infection-mediated pathological mechanism for AD is certainly one possibility for triggering an innate immune response in the CNS and subsequent production of antimicrobially active Aβ, other non-microbial factors may also be involved. Interestingly, peptides containing the microtubule binding sites on tau proteins have also been shown to harbor antimicrobial properties
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The role of AMP host cell cytoxicity in disease and defense is unclear. LL-37 cytotoxicity has been implicated in disease pathology [14] but may also have a normal function in antibody-dependent cell cytotoxicity, a host mechanism for the clearance of virus-infected and transformed cells [81]. At present Aβ's host cell cytotoxicity is only associated with disease. Identification of Aβ as an AMP raises the possibility that host cell cytotoxicity, or at least a component of this activity, may also have a role in innate immunity
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