**Robert P. Friedland 1,\*, Joseph D. McMillan <sup>2</sup> and Zimple Kurlawala <sup>3</sup>**


Received: 3 February 2020; Accepted: 26 February 2020; Published: 28 February 2020

**Abstract:** Despite the enormous literature documenting the importance of amyloid beta (Aβ) protein in Alzheimer's disease, we do not know how Aβ aggregation is initiated and why it has its unique distribution in the brain. In vivo and in vitro evidence has been developed to suggest that functional microbial amyloid proteins produced in the gut may cross-seed Aβ aggregation and prime the innate immune system to have an enhanced and pathogenic response to neuronal amyloids. In this commentary, we summarize the molecular mechanisms by which the microbiota may initiate and sustain the pathogenic processes of neurodegeneration in aging.

**Keywords:** Alzheimer's disease; microbiota; bacterial amyloid; FUBA; curli; CsgA; amyloid beta; neuroinflammation
