Alzheimer’s disease pathology programmed by gut-derived disparity: A
comprehensive understanding of neurodegeneration
Abstract
The human gut is colonized with microbial species that not only resides
but also facilitate in many functions. The alterations in this
gastrointestinal microbiota directly influence many body systems
including, central nervous system (CNS) disorders such as Alzheimer’s
disease (AD). The term microbiota is thus a determinant factor in the
association between illness and health. AD, the most common form of
dementia, is a neurodegenerative disorder associated with impaired
cognition and cerebral accumulation of amyloid-β peptides (Aβ).
Germ-free animals have provided enormous data on the existence of
dysbiosis and its conversion by fecal microbiota transplantation. The
main cause of AD is unknown and it is estimated that by 2050 the number
of patients will increase up to three times. Bacteria populating the gut
microbiota (GM) can secrete large amounts of amyloids and
lipopolysaccharides, which might contribute to the modulation of
signaling pathways and the production of proinflammatory cytokines
associated with the pathogenesis of AD. The Gut-brain axis links the
emotional and cognitive center of the brain with intestinal activities.
Thus, it can be said that the dysbiosis of human microbiome could be a
risk factor for AD. In this review, we provide an overview of GM and how
their dysregulation accounts for the pathogenesis of AD. Illustration of
the mechanisms underlying the modification of GM composition may pave
the way for developing novel preventive and therapeutic approach for AD.