Doc328,
Many thanks for your thorough and comprehensive response. It is both informative and helpful. I can now accept that Lilly may be well meaning rather than just greedy.
Pubmed is littered with research, documenting failures: studies featuring monoclonal antibodies destroying amyloid beta in order to cure Alzheimer’s disease. …. Probably in the order of a couple dozen during the last couple decades.
I don’t remember seeing one successful Phase 3 study, which was double blinded documented in PubMed.
There are also numerous studies going back to the late 1980s or early 1990s documenting a link between viruses (usually herpes) and Alzheimer’s disease.
When the viral attack is countered by the brain’s immune system, the visual result is an amyloid beta plaque and sometimes a Tau plaque.
While Alzheimer’s disease is normally correlated with a plaque, correlation is not proof of causation. It’s more likely that a virus which has incorporated itself into some of the brain’s neurons Is the root cause of the immune response and the resulting plaque.
The link between chickenpox and shingles is accepted, even though there’s a 40 year time lapse between the two. Is it really that much more difficult to believe there could be a link between herpes and Alzheimer’s disease which normally takes 50 to 60 years before it defeats the immune system.
Following is a PubMed abstract which reviews some of the virus/Alzheimer’s disease research in the last few decades of PubMed.
My very best regards,
Ian
Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts
Ruth F Itzhaki. FASEB J. 2017 Aug.
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Abstract
Support for the concept that herpes simplex virus type 1 (HSV1), when present in the brains of apolipoprotein E-e4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with over 120 publications providing direct or indirect evidence relevant to the hypothesis. No articles have contested the concept, apart from 3 published 13-18 yr ago. This review describes very recent studies on the role of HSV1 but refers also to older studies that provide background for some lesser-known related topics not covered in other recent reviews; these include the relevance of herpes simplex encephalitis and of epilepsy to AD, the action of IFN, and the possible relevance of the different types of DNA damage to AD-in particular, those caused by HSV1-and mechanisms of repair of damage. New epidemiologic data supporting previous studies on mild cognitive impairment and progression to AD are reviewed, as are those examining the relationship between total infectious burden (additive seropositivity to various microbes) and cognition/AD. The latter indicates the involvement of HSV1 and cytomegalovirus (and the necessity of taking into account any marked differences in sensitivity of antibody detection). Recent studies that provide further support for the occurrence of repeated reactivation of latent HSV1 in the brain in AD pathogenesis are also discussed.-Itzhaki, R. F. Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts.
Keywords: DNA repair; encephalitis; epidemiology; interferon; reactivation.
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