The amyloid-beta peptide forms insoluble clumps in the brains of patients with AD, and may be responsible for neuronal death (the amyloid hypothesis) . There have been many efforts to treat Alzheimers, most based on the dominant amyloid hypotheses. None have worked.
For quite a while, some have suspected that pathogens might be the primary cause of AD, but the idea has never been very popular with the funding agencies, or with most medical researchers. For example, there was some evidence that HSV-I increases Alzheimers risk, but there was a common objection: since healthy oldsters often have HSV-I in the brain, it can’t be the cause. In much the same way, many MDs said that h. pylori couldn’t be the cause of duodenal ulcers or stomach cancer, since it is found in large numbers of healthy people. It is the cause, though. Most people carrying the tuberculosis germ don’t get sick either – but nobody gets tuberculosis without it. In recent decades I think that few MDs say that therefore Mycobacterium tuberculosis is not really the cause of tuberculosis. Why don’t they? – the ‘logic’ is the same. I leave that as an exercise for my readers.
Some disease syndromes almost have to be caused by pathogens – for example, any with a fitness impact (prevalence x fitness reduction) > 2% or so, too big to be caused by mutational pressure. I don’t think that this is the case for AD: it hits so late in life that the fitness impact is minimal. However, that hardly means that it can’t be caused by a pathogen or pathogens – a big fraction of all disease syndromes are, including many that strike in old age. That possibility is always worth checking out, not least because infectious diseases are generally easier to prevent and/or treat.
There is new work that strongly suggests that pathogens are the root cause. It appears that the amyloid is an antimicrobial peptide. amyloid-beta binds to invading microbes and then surrounds and entraps them. ‘When researchers injected Salmonella into mice’s hippocampi, a brain area damaged in Alzheimer’s, A-beta quickly sprang into action. It swarmed the bugs and formed aggregates called fibrils and plaques. “Overnight you see the plaques throughout the hippocampus where the bugs were, and then in each single plaque is a single bacterium,” Tanzi says. ‘
If this new picture turns to to be correct, some combination of fighting & preventing the relevant pathogens, perhaps combined with methods of removing excessive amyloid buildup, would probably be fruitful.