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Host response: A trigger for neurodegeneration?

Nature Microbiology volume 1, Article number: 16129 (2016) Cite this article

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A new study provides clues to the physiological function of amyloid-β (Aβ), the plaque-forming peptide associated with Alzheimer's disease and finds a role for Aβ in fighting infection in the brain, by entangling pathogens in a web of amyloid fibrils. These data add to a growing appreciation of the role of microorganisms in neurodegenerative disease.

Within medicine, the fields of microbiology and neuroscience traditionally evolved on parallel trajectories with rare intersections. However, with the realization that a microbiota–gut–brain axis exists, this is now slowly changing1. Alzheimer's disease (AD) is the most common form of incurable dementia. On the cellular level, AD is characterized by the presence of extracellular aggregates of the amyloid-β peptide — termed Aβ plaques — and intracellular aggregates of tau protein — termed neurofibrillary tangles — in certain brain regions. Another hallmark of the disease is severe chronic neuroinflammation. Progressive neuronal loss and synapse degeneration have been attributed to each of these factors, individually or in concert, but the exact molecular mechanisms and causal chain of events that lead to AD remain elusive.

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Figure 1: A schematic of the hypothetical chain of events by which brain infection may lead to pathological amyloid-β peptide (Aβ) plaque formation in the brain.

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Authors and Affiliations

  1. Roman M. Stilling and John F. Cryan are at APC Microbiome Institute & Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland.,

    Roman M. Stilling & John F. Cryan

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  1. Roman M. Stilling
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  2. John F. Cryan
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Correspondence to John F. Cryan.

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Stilling, R., Cryan, J. Host response: A trigger for neurodegeneration?. Nat Microbiol 1, 16129 (2016). https://doi.org/10.1038/nmicrobiol.2016.129

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