6th Edition of Neurology World Conference 2026

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline, synaptic loss, and irreversible neuronal damage, affecting over 55 million people globally. It is primarily identified by amyloid-beta plaques and neurofibrillary tangles, with its progression inversely correlating with Brain-Derived Neurotrophic Factor (BDNF) levels. This literature review aims to address the central question of how gut microbial imbalances and intestinal barrier failures directly impact BDNF levels and cognitive decline, offering a fresh review to link gastrointestinal health to central nervous system pathology via the gut-brain axis (GBA). Since traditional approaches are plaque-centric, highlighting non-invasive GBA therapeutic solutions and early biomarkers is an urgent priority. By synthesizing literature on GBA inflammation, cytokine pathways, and data from clinical trials across PubMed and ScienceDirect within the last decade, this paper maps out the connection between gut dysbiosis and BDNF suppression to AD while evaluating therapeutic solutions on reducing GBA stress. The findings demonstrate that gut dysbiosis elevates circulating blood bacterial DNA (BB-DNA), triggering inflammation via pro-inflammatory cytokines that suppress BDNF transcription and downregulate its primary receptor (TrKB). Additionally, the data revealed that targeted therapeutic solutions, including probiotics, physical exercise, and anti-inflammatory diets, successfully reduced oxidative stress, minimized microglia activation, and elevated BDNF to preserve cognitive function. Ultimately, BB-DNA and BDNF levels provide non-invasive biomarker profiles to track GBA-related neurodegeneration and future studies should aim to investigate how an AD patient’s baseline gut microbiome health can dictate their individual responses to targeted treatments.