Microbial BMAA elicits mitochondrial dysfunction, innate immunity activation, and Alzheimer's disease features in cortical neurons.

ABSTRACT:

Background

After decades of research recognizing it as a complex multifactorial disorder, sporadic Alzheimer's disease (sAD) still has no known etiology. Adding to the myriad of different pathways involved, bacterial neurotoxins are assuming greater importance in the etiology and/or progression of sAD. β-N-Methylamino-L-alanine (BMAA), a neurotoxin produced by some microorganisms namely cyanobacteria, was previously detected in the brains of AD patients. Indeed, the consumption of BMAA-enriched foods has been proposed to induce amyotrophic lateral sclerosis-parkinsonism-dementia complex (ALS-PDC), which implicated this microbial metabolite in neurodegeneration mechanisms.

Methods

Freshly isolated mitochondria from C57BL/6 mice were treated with BMAA and O₂ consump

SUBMITTER: Silva DF 

PROVIDER: S-EPMC7643281 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature