Abstract
Alzheimer’s disease (AD) is an incurable, neuropsychiatric, pathological condition that deteriorates the worth of geriatric lives. AD is characterized by aggregated senile amyloid plaques, neurofibrillary tangles, neuronal loss, gliosis, oxidative stress, neurotransmitter dysfunction, and bioenergetic deficits. The changes in GIT composition and harmony have been recognized as a decisive and interesting player in neuronal pathologies including AD. Microbiota control and influence the oxidoreductase status, inflammation, immune system, and the endocrine system through which it may have an impact on the cognitive domain. The altered and malfunctioned state of microbiota is associated with minor infections to complicated illnesses that include psychosis and neurodegeneration, and several studies show that microbiota regulates neuronal plasticity and neuronal development. The altered state of microbiota (dysbiosis) may affect behavior, stress response, and cognitive functions. Chronic stress-mediated pathological progression also has a well-defined role that intermingles at various physiological levels and directly impacts the pathological advancement of AD. Chronic stress-modulated alterations affect the well-established pathological markers of AD but also affect the gut–brain axis through the mediation of various downstream signaling mechanisms that modulate the microbial commensals of GIT. The extensive literature reports that chronic stressors affect the composition, metabolic activities, and physiological role of microbiota in various capacities. The present manuscript aims to elucidate mechanistic pathways through which stress induces dysbiosis, which in turn escalates the neuropathological cascade of AD. The stress–dysbiosis axis appears a feasible zone of work in the direction of treatment of AD.
Highlights
Increased age, owing to medical advancement, has made humans prone to a variety of complications and illnesses
The probiotic supplementation of VSL#3 to aged rats induced a robust perturbation in gut microbiota composition, which was accompanied by gene expression changes in the brain cortex, attenuated age-related deficits in long-term potentiation, decreased microglial activation, and increased brain-derived neurotrophic factor (BDNF) and synapsin levels [138]
Microbiota influence the neuropathological cascade of Alzheimer’s disease (AD) and microbiota modulation has shown encouraging results, including the reduction of amyloid plaques and neurofibrillary tangles, alleviation of glial responses, and improvement in cognitive performance
Summary
Increased age, owing to medical advancement, has made humans prone to a variety of complications and illnesses. Gut microbes influence brain attributes through various ways, which include dysbiosis-related inflammation, the involvement of altered microbiota in oxidative stress, altered permeability, resultant immune activity, age-related reduction in beneficial microbiota, dysbiosis induced insulin-resistant state, etc. These are the major mechanistic and pathological links through which cognitive domain and pathological progression of AD are influenced [13]. These observations points toward the impact of peripheral inflammation- and oxidative stress-induced apoptotic cascade in brain regions that may be responsible for neuronal demise [23]
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