The study of Soscia et al documents that Amyloid β-Protein has antimicrobial effect is interesting and the importance of the study are supported by findings of elevated immune activation in Alzheimer`s disease (AD) (1).
In the Soscia study the most pronounced antibiotic effect of Amyloid β-Protein was seen against Candida Albicans. This infective agent is amongst many microbes that elevates activity of the immune mediator tumour necrosis factor-alpha (TNF) (2). It has recently become clear that such immune activation has a general negative impact on cognition (3, 4). Healthy persons with high levels of TNF have elevated risk of developing AD (5) and elevated TNF confers a risk for mild cognitive decline developing into dementia (6). Patients that already have been diagnosed with AD has also have elevated TNF (7). In accordance with these studies of systemic immune activation, post-mortem studies of brain tissue from AD patients show elevated activity in the TNF-pathways (8).

As elevated levels of TNF is associated with negative impact on cognition and confers risk of AD, it has been suggested that antagonizing TNF might be a treatment option (9). Treatment with a TNF-blocking agent has also been tried in an AD patient and were found to have a rapid effect improving some cognitive measures (10). The long term effect of such treatment is uncertain. Importantly, immune suppression is not a good treatment option if the elevated immune activation in is due to an infective agent. In such a case an immune suppressant would make the immune response even more ineffective.
And as mentioned in the comment by Ruth Itzhaki, there are indications that infections elevate the risk of Alzheimer (11-13). It has also been reported that blocking the immune response is associated with more rapid progression in animal models of AD (14, 15).
The fact that Amyloid β-Protein is an antimicrobial peptide supports the hypothesis that immune activation might be caused by subclinical chronic infection. Thus, treatment trials with antibiotic agents might be a better alternative in AD than treatment trials with immune blocking agents.


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